Genome complexity in embryology (Introduction)

by David Turell @, Friday, May 10, 2013, 14:53 (3976 days ago)
edited by unknown, Friday, May 10, 2013, 15:04

DNA goes through contortions to make a living person:-http://www.sciencedaily.com/releases/2013/05/130509123647.htm-http://phys.org/news/2013-05-salk-epigenomics-stem-cells-mimic.html

Genome complexity: transposon control

by David Turell @, Monday, June 24, 2013, 15:55 (3931 days ago) @ David Turell

Transposons control or change some mutations. These are the 'jumping genes' and like all of bological life, there are feedback control loops tp manage what could be a runaway process:-http://www.sciencedaily.com/releases/2013/06/130620132221.htm

Genome complexity: copy control

by David Turell @, Monday, June 24, 2013, 16:06 (3931 days ago) @ David Turell

"Only about 15 percent of the human genome consists of protein-coding genes, but in recent years scientists have found that a surprising amount of the junk, or intergenic DNA, does get copied into RNA—the molecule that carries DNA's messages to the rest of the cell.
 
Scientists have been trying to figure out just what this RNA might be doing, if anything. In 2008, MIT researchers led by Institute Professor Phillip Sharp discovered that much of this RNA is generated through a process called divergent expression, through which cells read their DNA in both directions moving away from a given starting point." -
Read more at: http://phys.org/news/2013-06-biologists-reveal-cells-genome.html#jCp

Genome complexity: 3-D arrangement

by David Turell @, Monday, June 24, 2013, 16:10 (3931 days ago) @ David Turell

"Imagine a long and immensely convoluted grape vine, its twisted branches presenting some grapes to be plucked easily, while concealing others beyond reach," said Dr Mercer. "At the same time, imagine a lazy fruit picker only picking the grapes within easy reach.
 
"The same principle applies in the genome. Specific genes and even specific exons, are placed within easy reach by folding."
 
"Over the last few years, we've been starting to appreciate just how the folding of the genome helps determine how it's expressed and regulated,"
 
"This study provides the first indication that the three-dimensional structure of the genome can influence the splicing of genes."
 
"We can infer that the genome is folded in such a way that the promoter region—the sequence that initiates transcription of a gene—is located alongside exons, and they are all presented to transcription machinery."
 
"This supports a new way of looking at things, one that the genome is folded around transcription machinery, rather than the other way around. Those genes that come in contact with the transcription machinery get transcribed, while those parts which loop away are ignored."-
 Read more at: http://phys.org/news/2013-06-genome-3d-genes.html#jCp

Genome complexity: ribosome mechanics

by David Turell @, Sunday, June 30, 2013, 00:46 (3926 days ago) @ David Turell

A subunit rotates and a protein is made part by part from decoding the DNA bases presented by the messenger RNA:-"Translocation involves two steps (as Noller's lab showed back in 1989). Step one is the movement of the tRNA's "acceptor end" (where it carried the amino acid). This leads to a hybrid state, with the two ends of the tRNA in two different sites on the ribosome: the "anticodon end" is still lined up with the matching mRNA codon in one site, while the acceptor end has moved on to the next site. Step two is the movement of the tRNA's anticodon end together with the messenger RNA, which advances by one codon. Step two requires a catalyst called elongation factor G (EF-G). The new study shows the ribosome in the middle of step two, with EF-G bound to it and the tRNA halfway between the hybrid state and the final state.-"This is one of the most fundamental movements in all of biology, at the root of the whole mechanism for translation of the genetic code, and we now understand it all the way down to the molecular level," Noller said. "This mechanism had to be in place around the origin of life as we know it."-http://www.sciencedaily.com/releases/2013/06/130627142400.htm-
My bold. Think of the implications. This was present with the first fully developed cells.

Genome complexity: copying at work

by David Turell @, Thursday, July 04, 2013, 02:01 (3922 days ago) @ David Turell

Genome complexity: copying at work

by dhw, Thursday, July 04, 2013, 13:04 (3921 days ago) @ David Turell

http://www.youtube.com/watch?feature=player_embedded&v=gdBJt6sdDfI
 
 
DAVID: Darwin would discard his theories if he could see this.-More fascinating stuff, for which many thanks. But which theories would Darwin discard? Common descent? Natural selection? The "intelligent genome" so vividly illustrated here might well have made him change his views on how evolution works, especially in the domain of innovation, but he himself anticipated that: "A grand and almost untrodden field of inquiry will be opened, on the causes and laws of variation, on correlation of growth, on the effects of use and disuse, on the direct action of external conditions, and so forth." (Recapitulation and Conclusion) Does the modern study of genetics tell us that evolution didn't happen?

Genome complexity: copying at work

by David Turell @, Thursday, July 04, 2013, 16:05 (3921 days ago) @ dhw

dhw: Does the modern study of genetics tell us that evolution didn't happen?-It presumes that evolution happened, but there is so much that is unexplained, and no evidence that it is not guided and directed, which would be very difficult to detect. Remember we are trying to recover history from millions of yers ago.

Genome complexity: copying at work

by dhw, Friday, July 05, 2013, 12:59 (3920 days ago) @ David Turell

http://www.youtube.com/watch?feature=player_embedded&v=gdBJt6sdDfI-DAVID: Darwin would discard his theories if he could see this.-Dhw: More fascinating stuff, for which many thanks. But which theories would Darwin discard? Common descent? Natural selection? [...] Does the modern study of genetics tell us that evolution didn't happen?-DAVID: It presumes that evolution happened, but there is so much that is unexplained, and no evidence that it is not guided and directed, which would be very difficult to detect. Remember we are trying to recover history from millions of years ago.-Yes indeed, there is so much that is unexplained ... as Darwin himself readily acknowledged ... and there is no evidence that it is or that it is not guided and directed, but that has nothing to do with Darwin's theories. And yes indeed, we are trying to recover history from millions of years ago, and Darwin never said we weren't. I still see no reason why Darwin and we ourselves should discard the theories of common descent, natural selection and evolution because of genetics.

Genome complexity: copying at work

by David Turell @, Friday, July 05, 2013, 15:29 (3920 days ago) @ dhw


> dhw:Yes indeed, there is so much that is unexplained ... as Darwin himself readily acknowledged ... and there is no evidence that it is or that it is not guided and directed, but that has nothing to do with Darwin's theories. And yes indeed, we are trying to recover history from millions of years ago, and Darwin never said we weren't. I still see no reason why Darwin and we ourselves should discard the theories of common descent, natural selection and evolution because of genetics.-I'm not asking that we remove ourselves from a recognition of evolution by common descent mediated by natural selection. Darwin is interpreted as permitting the idea that he has explained it as occurring totally by a chance mechanism, when the enormous layer upon layer of complexity of the genome belies that idea. There is intellect and planning behind all of it.

Genome complexity: copying DNA at work

by David Turell @, Monday, July 15, 2013, 15:29 (3910 days ago) @ David Turell

How helicase acts as a moleclar machine:-http://phys.org/news/2013-07-key-molecular-duplicates-dna-deciphered.html

Genome complexity: SNP\'s

by David Turell @, Monday, July 29, 2013, 17:36 (3896 days ago) @ David Turell

Can make a tremendous difference:-"Scientists at Rice University and the University of Washington (UW) this week unveiled a groundbreaking new method for detecting minute changes known as single nucleotide polymorphisms (SNPs) in the human genome. The human genome has more than 6 billion base pairs, and one of the revelations of modern genomics is that even the slightest change in the sequence—a single-nucleotide difference—can have profound effects."-"Scientists have sequenced the genomes of dozens of species, but those species-level genomes only tell part of the genetic story for a given individual. In people, for example, slight differences in just a few nucleotides can mean the difference between having green or brown eyes. This type of genetic variation within a species is called polymorphism, and SNPs are the smallest unit of polymorphic variation."-http://medicalxpress.com/news/2013-07-quadratic-smallest-genetic.html

Genome complexity: why only 20 essential amino acids

by David Turell @, Monday, May 02, 2016, 19:18 (2888 days ago) @ David Turell

New theoretical research into transfer RNA shows that the required shape of the tRNA limits the genome to only 20 coding amino acids:-http://phys.org/news/2016-05-discovery-fundamental-limit-evolution-genetic.html-
"A study performed at IRB Barcelona offers an explanation as to why the genetic code stopped growing 3,000 million years ago. This is attributed to the structure of transfer RNAs—the key molecules in the translation of genes into proteins. The genetic code is limited to 20 amino acids—the building blocks of proteins—the maximum number that prevents systematic mutations, which are fatal for life. The discovery could have applications in synthetic biology. -"Nature is constantly evolving—its limits determined only by variations that threaten the viability of species. Research into the origin and expansion of the genetic code are fundamental to explain the evolution of life. In Science Advances, a team of biologists specialised in this field explain a limitation that put the brakes on the further development of the genetic code, which is the universal set of rules that all organisms on Earth use to translate genetic sequences of nucleic acids (DNA and RNA) into the amino acid sequences that comprise the proteins that undertake cell functions.-***-"the genetic code evolved to include a maximum of 20 amino acids and that it was unable to grow further because of a functional limitation of transfer RNAs—the molecules that serve as interpreters between the language of genes and that of proteins. This halt in the increase in the complexity of life happened more than 3,000 million years ago, before the separate evolution of bacteria, eukaryotes and archaebacteria, as all organisms use the same code to produce proteins from genetic information.-"The authors of the study explain that the machinery that translates genes into proteins is unable to recognise more than 20 amino acids because it would confuse them, which would lead to constant mutations in proteins and thus the erroneous translation of genetic information "with catastrophic consequences", in Ribas' words. "Protein synthesis based on the genetic code is the decisive feature of biological systems and it is crucial to ensure faithful translation of information," says the researcher."
 
***
 -"Saturation of the genetic code has its origin in transfer RNAs (tRNAs), the molecules responsible for recognising genetic information and carrying the corresponding amino acid to the ribosome, the place where chain of amino acids are made into proteins following the information encoded in a given gene. However, the cavity of the ribosome into which the tRNAs have to fit means that these molecules have to adopt an L-shape, and there is very little possibility of variation between them. "It would have been to the system's benefit to have made new amino acids because, in fact, we use more than the 20 amino acids we have, but the additional ones are incorporated through very complicated pathways that are not connected to the genetic code. And there came a point when Nature was unable to create new tRNAs that differed sufficiently from those already available without causing a problem with the identification of the correct amino acid. And this happened when 20 amino acids were reached," explains Ribas."-Comment: If God is the designer, the chemistry limits Him!

Genome complexity: double coding

by David Turell @, Thursday, July 04, 2013, 18:08 (3921 days ago) @ dhw

A gene is found tht codes for two different proteins at the same time:-http://www.sciencedaily.com/releases/2013/07/130703120554.htm

Genome complexity: 3-D arrangement

by David Turell @, Wednesday, March 15, 2017, 14:33 (2571 days ago) @ David Turell

Now visualized in mammalian cells:

https://www.sciencedaily.com/releases/2017/03/170313135018.htm

"Scientists have determined the first 3D structures of intact mammalian genomes from individual cells, showing how the DNA from all the chromosomes intricately folds to fit together inside the cell nuclei

" Using their new approach, the researchers have now been able to determine the structures of active chromosomes inside the cell, and how they interact with each other to form an intact genome. This is important because knowledge of the way DNA folds inside the cell allows scientists to study how specific genes, and the DNA regions that control them, interact with each other. The genome's structure controls when and how strongly genes -- particular regions of the DNA -- are switched 'on' or 'off'. This plays a critical role in the development of organisms and also, when it goes awry, in disease.

***

"Professor Ernest Laue, whose group at Cambridge's Department of Biochemistry developed the approach, commented: "Knowing where all the genes and control elements are at a given moment will help us understand the molecular mechanisms that control and maintain their expression.

"'In the future, we'll be able to study how this changes as stem cells differentiate and how decisions are made in individual developing stem cells. Until now, we've only been able to look at groups, or 'populations', of these cells and so have been unable to see individual differences, at least from the outside. Currently, these mechanisms are poorly understood and understanding them may be key to realising the potential of stem cells in medicine."

***

"Dr Tom Collins from Wellcome's Genetics and Molecular Sciences team said: "Visualising a genome in 3D at such an unprecedented level of detail is an exciting step forward in research and one that has been many years in the making. This detail will reveal some of the underlying principles that govern the organisation of our genomes -- for example how chromosomes interact or how structure can influence whether genes are switched on or off. If we can apply this method to cells with abnormal genomes, such as cancer cells, we may be able to better understand what exactly goes wrong to cause disease, and how we could develop solutions to correct this.'"

Comment: As before the 3-D relationships control how genes are expressed and affect each other when they are in close proximity. It is another layer of genome complexity.

Genome complexity: 3-D arrangement in bacteria

by David Turell @, Thursday, March 23, 2017, 23:40 (2563 days ago) @ David Turell

Now shown in single celled animals:

https://www.sciencedaily.com/releases/2017/03/170323132532.htm

"Researchers have described the 3D structure of the genome in the extremely small bacteria Mycoplasma pneumoniae. They discovered previously unknown arrangements of DNA within this tiny bacteria, which are also found in larger cells. Their findings suggest that this type of organization is a universal feature of living cells.

***

"Notably, the CRG team, which counted with the expertise in Mycoplasma from the Serrano's laboratory and the collaboration of the ICREA research professor Marc Marti-Renom at CNAG-CRG, discovered that Mycoplasma's circular chromosome is consistently organised the same way in all the cells, with a region called the Origin (where DNA copying begins) at one end of the structure and the midpoint of the chromosome located at the opposite end. This is a similar arrangement to that seen in some other larger bacterial species.

"Intriguingly, the CRG team found that even the tiny Mycoplasma chromosome is organised into distinct structural domains, each containing genes that are also turned on or off in a co-ordinated way.

"Marie Trussart, the lead author on the paper, said: "Studying bacteria with such a small genome was a big technical challenge, especially because we were using super-resolution microscopy, and it took us five years to complete the project. We had suspected that the Mycoplasma genome might have a similar overall organisation to other bacteria, but we were completely surprised to find that it was also organised into domains, which can be considered as regulatory units of chromatin organisation and that we had identified a previously unknown layer of gene regulation. This research shows that the organisation and control of genes cannot be understood by just looking at the linear sequence of DNA in the genome. Indeed, to get the full picture of gene regulation we need to look at the three-dimensional organisation of the chromatin that also coordinates gene activity."

"The discovery suggests that this level of organisation and genetic control is common to all living cells, from the largest to the smallest, and can be achieved with little more than a handful of DNA binding proteins and the structural properties of the DNA itself."

Comment: Another example of the importance of 3-D DNA relationships. Looks like design.

Genome complexity: copy control

by David Turell @, Saturday, August 03, 2013, 15:27 (3891 days ago) @ David Turell

It seems that even in the copying control systems there are exceptions. Introns and stop codons are sometimes kept which will change gene expression:-http://www.sciencedaily.com/releases/2013/08/130802101900.htm

Genome complexity: Shapiro review

by David Turell @, Wednesday, August 07, 2013, 02:07 (3888 days ago) @ David Turell

Very exhaustive coverage with pages and pages of references:-"The preceding discussion presents a large but far from exhaustive catalogue of
molecular tools that cells possess to make controlled inscriptions in their genomes over all biological time scales. The empirical evidence for biological action in hereditary genome changes has become so overwhelming that it is surprising how widespread the notion of accidental change still remains. (my bold)-"There is broad recognition that cells have elaborate molecular regulatory circuits and DNA formatting (section 1) to control the timing and location of genome movements,replication, expression and repair [13]. These events occur at the shortest biological time scale. Although we know less of the details, there is a similar recognition that epigenetic chromatin formatting is subject to a comparable regulatory regime at intermediate biological time scales [254, 255].
However, there is virtually no recognition that the longest-term genome inscriptions by DNA restructuring are subject to cellular control circuits. The reasons for this confusion are philosophical rather than empirical. They date back to the evolutionary debates of the late 19th and early 20th Centuries. These philosophical prejudices notwithstanding, the empirical data is
clear that DNA changes are equally subject to short-term and epigenetic regulation."-http://shapiro.bsd.uchicago.edu/Shapiro.2013.How%20Life%20Changes%20Itself-%20The%20Read-Write%20(RW)%20Genome.Physics%20of%20Life%20Reviews.pdf

Genome complexity: another example

by David Turell @, Wednesday, August 07, 2013, 18:44 (3887 days ago) @ David Turell

Careful copying and exclusion of mistakes:-http://www.the-scientist.com//?articles.view/articleNo/36679/title/Shushing-RNA/

Genome complexity: Shapiro review

by David Turell @, Thursday, August 08, 2013, 15:08 (3886 days ago) @ David Turell

Shapiro's message that orgnisms tend to make automatic adjustments to their DNA to adapt to challenges most likely creates the mess that is the genomic tree of life: gene studies don't lead to proper trees!-http://www.wired.com/wiredscience/2013/06/algorithms-revise-tree-of-lif/2/-"According to a new study partly focused on yeast, the conflicting picture from individual genes is even broader than scientists suspected. "They report that every single one of the 1,070 genes conflicts somewhat," said Michael Donoghue, an evolutionary biologist at Yale who was not involved in the study. "We are trying to figure out the phylogenetic relationships of 1.8 million species and can't even sort out 20 [types of] yeast," he said"

Genome complexity: Using RNAi in research

by David Turell @, Wednesday, August 14, 2013, 18:34 (3880 days ago) @ David Turell

Naturally occurring interference RNA is used in research to sort ouT genes and their function. This shows another view of how complex the genome is.-
http://www.the-scientist.com//?articles.view/articleNo/36692/title/Gene-Silencing-Is-Golden/

Genome complexity: RNA disposal

by David Turell @, Friday, August 16, 2013, 16:06 (3878 days ago) @ David Turell

Defective and unneeded RNA's are disposed of:-http://phys.org/news/2013-08-rnas-molecular-shredder-scientists-unravel.html

Genome complexity: useful transposons

by David Turell @, Friday, August 16, 2013, 22:37 (3878 days ago) @ David Turell

Transposons were thought to be reproducing junk in DNA. Instead it now appears they have an epigenetic role, in this case to improve immunity. It strongly suggests they will have other important roles:-http://www.sciencedaily.com/releases/2013/08/130815113723.htm

Genome complexity: useful transposons

by David Turell @, Friday, August 16, 2013, 23:55 (3878 days ago) @ David Turell

Quotes from the article:-"Transposons are DNA elements that can multiply and change their location within an organism's genome. Discovered in the 1940s, for years they were thought to be unimportant and were called "junk DNA."-"While it has been known for a while that transposon insertions can have positive effects for their respective host organisms and accelerate evolution of their hosts, cases of such adaptive transposon insertions have been rarely documented and are, so far, poorly understood."-"It would make sense to assume that at other transposons, H3K9me2 levels are also modulated during immune responses and that this epigenetic mark affects the activity of other genes that are important for plant immunity," Eulgem said. "If this is true, we have uncovered a completely new genetic -- or epigenetic -- mechanism that allows plants to sense that they are under pathogen attack and to initiate appropriate immune responses.'"-http://www.sciencedaily.com/releases/2013/08/130815113723.htm

Genome complexity: pseudogenes

by David Turell @, Tuesday, August 20, 2013, 15:48 (3874 days ago) @ David Turell

Pseudogenes are not pseudo, but very useful elements in the genome. Less junk, more function:-http://designed-dna.org/blog/files/c618328523fff8d1b860267f05417554-80.php

Genome complexity: pseudogenes

by dhw, Wednesday, August 21, 2013, 13:24 (3873 days ago) @ David Turell

David: Pseudogenes are not pseudo, but very useful elements in the genome. Less junk, more function:-http://designed-dna.org/blog/files/c618328523fff8d1b860267f05417554-80.php-QUOTE: "Pseudogenes are clearly not pseudo, but rather complex sections of genetic code programmed by an omnipotent and all-wise Creator. The only thing that is pseudo, is the failed paradigm of evolution."-If junk DNA is not junk, how does that prove evolution is a failed paradigm? The evolutionist can simply argue that natural selection has got rid of all the DNA that WAS junk. And who says that the Theory of Evolution runs contrary to a complex genetic code programmed by a Creator? Maybe a Creator created a complex genetic code that would enable single-celled creatures to evolve into us wonderful humans. And if junk and pseudogenes do exist, what does that tell us? Maybe godless evolution left odd bits and pieces lying around, or divine evolution left odd bits and pieces lying around. It might seem strange for an omnipotent and all-wise Creator of each individual "kind" to leave odd bits and pieces lying around, but who says he's omnipotent and all-wise? Both sides of the argument seem like a load of junk to me.

Genome complexity: pseudogenes

by David Turell @, Wednesday, August 21, 2013, 16:38 (3873 days ago) @ dhw


> dhw:If junk DNA is not junk, how does that prove evolution is a failed paradigm? The evolutionist can simply argue that natural selection has got rid of all the DNA that WAS junk. And who says that the Theory of Evolution runs contrary to a complex genetic code programmed by a Creator? -The argument is more complex than that. Junk has been used to say that natural selection discarded stuff throughout purposeless chance evoluton. The current findings remove much of the junk label and demonstrate that DNA must be viewed in an 3-D perspective, with the questionable material being found to have modifying fuctions or acting as 3-D spacers to bring other modifiers close to the genes they are acting upon. The latter implies purposeful junk and fits the concept of theistic evolution.

Genome complexity: pseudogenes

by dhw, Thursday, August 22, 2013, 12:46 (3872 days ago) @ David Turell

dhw: If junk DNA is not junk, how does that prove evolution is a failed paradigm? The evolutionist can simply argue that natural selection has got rid of all the DNA that WAS junk. And who says that the Theory of Evolution runs contrary to a complex genetic code programmed by a Creator? -DAVID: The argument is more complex than that. Junk has been used to say that natural selection discarded stuff throughout purposeless chance evoluton.
 
I thought the atheist point was that so-called junk DNA (i.e. those existing elements of DNA that are of no use) proved that life was not the product of design, since a designer would not create anything useless (or at least an "omnipotent, all-wise Creator" wouldn't). If now it's proved that some is junk and some isn't, both sides can claim partial support; if none of it is junk, atheist evolutionists can claim natural selection has streamlined DNA, theists can claim that God has streamlined DNA, and theist evolutionists can claim that God designed DNA in such a way that natural selection would streamline it. It doesn't matter what we discover about Nature, the information can always be twisted to fit the theory.

Genome complexity: pseudogenes

by David Turell @, Thursday, August 22, 2013, 14:53 (3872 days ago) @ dhw

dhw: If junk DNA is not junk, how does that prove evolution is a failed paradigm? 
> DAVID: The argument is more complex than that. Junk has been used to say that natural selection discarded stuff throughout purposeless chance evoluton.
> 
> dhw: I thought the atheist point was that so-called junk DNA (i.e. those existing elements of DNA that are of no use) proved that life was not the product of design, since a designer would not create anything useless (or at least an "omnipotent, all-wise Creator" wouldn't). If now it's proved that some is junk and some isn't, both sides can claim partial support;-You are still missing a major point. Years ago more than 90% of DNA was thought to be junk. Now many scientists support the idea that up to 80% is not junk. As research into DNA becomes more and more refined it seems that junk disappears and more and more DNA appears purposeful. If recognized junk becomes only a tiny percentage of DNA where does the atheist argument devolve to?

Genome complexity: pseudogenes

by dhw, Friday, August 23, 2013, 10:50 (3871 days ago) @ David Turell

dhw: If junk DNA is not junk, how does that prove evolution is a failed paradigm? -DAVID: Junk has been used to say that natural selection discarded stuff throughout purposeless chance evoluton.-dhw: I thought the atheist point was that so-called junk DNA (i.e. those existing elements of DNA that are of no use) proved that life was not the product of design, since a designer would not create anything useless (or at least an "omnipotent, all-wise Creator" wouldn't). If now it's proved that some is junk and some isn't, both sides can claim partial support;-DAVID: You are still missing a major point. Years ago more than 90% of DNA was thought to be junk. Now many scientists support the idea that up to 80% is not junk. As research into DNA becomes more and more refined it seems that junk disappears and more and more DNA appears purposeful. If recognized junk becomes only a tiny percentage of DNA where does the atheist argument devolve to?-Perhaps you overlooked the rest of my post! Let me repeat it for you:
"[...] if none of it is junk, atheist evolutionists can claim natural selection has streamlined DNA, theists can claim that God has streamlined DNA, and theist evolutionists can claim that God designed DNA in such a way that natural selection would streamline it. It doesn't matter what we discover about Nature, the information can always be twisted to fit the theory."

Genome complexity: smORFs and lncRNA

by David Turell @, Friday, August 23, 2013, 15:32 (3871 days ago) @ dhw

Yipes: more unnoticed tiny genes:-http://www.the-scientist.com//?articles.view/articleNo/37159/title/Hidden-Treasures/

Genome complexity: pseudogenes

by David Turell @, Friday, August 23, 2013, 17:59 (3871 days ago) @ dhw


> dhw: Perhaps you overlooked the rest of my post! Let me repeat it for you:
> "[...] if none of it is junk, atheist evolutionists can claim natural selection has streamlined DNA, theists can claim that God has streamlined DNA, and theist evolutionists can claim that God designed DNA in such a way that natural selection would streamline it. It doesn't matter what we discover about Nature, the information can always be twisted to fit the theory."-You persist in missing the point, which is why I have ignored the above. The evolutionists point to junk as proof of evolution. Lots of inventive mutations discarded in the process of evolutionary development, creating a huge pile of DNA junk, which then 'proves' evoluton happened from the debris left behind. The discovery of functional material in 80% of DNA, and the realization of spacer material (3-D) has the confirmed atheistic evolutionists screaming and yelling (read Larry Moran's blog as an example) makes DNA look very designed and supports the idea of theistic evolution. Natural selection has streamlined nothing. DNA is a huge complex structure with all sorts of partially hidden controls.-And you are right about twisting. Dawkins is doing just that. He has quotes saying that junk proves evolution and newer quotes which tell us, the lack of junk proves evolution.

Genome complexity: pseudogenes

by dhw, Saturday, August 24, 2013, 12:23 (3870 days ago) @ David Turell

DAVID: If recognized junk becomes only a tiny percentage of DNA where does the atheist argument devolve to? -dhw: Perhaps you overlooked the rest of my post! Let me repeat it for you:
"[...] if none of it is junk, atheist evolutionists can claim natural selection has streamlined DNA, theists can claim that God has streamlined DNA, and theist evolutionists can claim that God designed DNA in such a way that natural selection would streamline it. It doesn't matter what we discover about Nature, the information can always be twisted to fit the theory."-DAVID: You persist in missing the point, which is why I have ignored the above. The evolutionists point to junk as proof of evolution. Lots of inventive mutations discarded in the process of evolutionary development, creating a huge pile of DNA junk, which then 'proves' evoluton happened from the debris left behind. [...] 
And you are right about twisting. Dawkins is doing just that. He has quotes saying that junk proves evolution and newer quotes which tell us, the lack of junk proves evolution.-You asked what the atheist argument would be if it was proved that junk DNA was not junk, and I told you. Just for the record, Dawkins' miraculous, even hilarious U-turn was as follows: "I have noticed that there are some creationists who are jumping on [the ENCODE results] because they think that's awkward for Darwinism. Quite the contrary it's exactly what a Darwinist would hope for, to find usefulness in the living world...." (Interview with Rabbi Sacks) That's what I meant by natural selection streamlining DNA (it retains what is useful). The report on the interview also tells us what Dawkins said before his volte face: "It stretches even their [Creationists'] creative ingenuity to make a convincing reason why an intelligent designer should have created a pseudogene -- a gene that does absolutely nothing and gives every appearance of being a superannuated version of a gene that used to do something -- unless he was deliberately setting out to fool us." That's the previous atheist argument I was referring to in my post.
 
I gather that ENCODE'S findings are still in dispute, but obviously I'm in no position to take sides. For the sake of argument, though, I'm quite prepared to accept that 80% or even 100% of "junk" is not junk. My point here is that it won't make people change their basic beliefs, and there's no reason why it should. When common descent first hit the headlines, what did believers do? They either refused to accept the theory, or adapted their beliefs to incorporate it. Similarly now, atheists either reject the DNA findings or adapt them to Darwinism. And so I stand by the two points I have made during this discussion: 1) Even if there is no junk, this does not in any way justify the claim made in the article that evolution is "a failed paradigm"; 2) It doesn't matter what we discover about Nature, the information can always be twisted to fit the theory. To which I would add, none of us know which theory is correct.

Genome complexity: pseudogenes

by David Turell @, Saturday, August 24, 2013, 15:56 (3870 days ago) @ dhw

dhw:The report on the interview also tells us what Dawkins said before his volte face: "It stretches even their [Creationists'] creative ingenuity to make a convincing reason why an intelligent designer should have created a pseudogene -- a gene that does absolutely nothing and gives every appearance of being a superannuated version of a gene that used to do something -- unless he was deliberately setting out to fool us." That's the previous atheist argument I was referring to in my post.-The problem with this Dawkins quote,and it makes it obvious Dawkins is not keeping up with the reseach, pseudogenes are now beingfound to have functional abilities. An atheist argument with no basis. And that has been my point. I fully accept your view that minds set in cement will not change, but if a clear thinker follows what is happening, junk disappearing is removing part of the atheists present theory about chance controlling DNA development.
> 
> dhw: I gather that ENCODE'S findings are still in dispute, but obviously I'm in no position to take sides. ..... To which I would add, none of us know which theory is correct.-The debate as I follow Shapiro and Moran favors Shapiro. The findings are making most of DNA more and more functional, and much more complex. Complexity is anti-chance!

Genome complexity: introns and splicosomes

by David Turell @, Saturday, August 24, 2013, 23:24 (3870 days ago) @ David Turell
edited by unknown, Saturday, August 24, 2013, 23:38

Activating a gene and controlling its expression involves deleting large and small introns (spacers)using major and minorsplicosomes and controlled by RNA:-http://www.uphs.upenn.edu/news/News_Releases/2013/08/dreyfuss/-Carefully read the article to appreciate the complexity of tight controls over gene expression.-My argument remains the same. The more complex the genome mechanisms are shown to be, the less likely chance did it, and the more likely it was designed. It is death by small strokes to the atheist version of evolution as research advances. Funny, but the complexity keeps getting more complex with every advance. And will obviously continue to do so. The atheists won't give up by logical folks can se the end point. Chance doesn't have a chance to be correct.

Genome complexity: pseudogenes

by dhw, Sunday, August 25, 2013, 20:54 (3869 days ago) @ David Turell

dhw:The report on the interview also tells us what Dawkins said before his volte face: "It stretches even their [Creationists'] creative ingenuity to make a convincing reason why an intelligent designer should have created a pseudogene -- a gene that does absolutely nothing and gives every appearance of being a superannuated version of a gene that used to do something -- unless he was deliberately setting out to fool us." That's the previous atheist argument I was referring to in my post.-DAVID: The problem with this Dawkins quote,and it makes it obvious Dawkins is not keeping up with the reseach, pseudogenes are now beingfound to have functional abilities. An atheist argument with no basis. And that has been my point. I fully accept your view that minds set in cement will not change, but if a clear thinker follows what is happening, junk disappearing is removing part of the atheists present theory about chance controlling DNA development.-This quote was BEFORE the latest research, and Dawkins is now arguing that if junk is not junk, that fits in with Darwinism. And of course in one sense it does (see below), even if his apparently unacknowledged U-turn makes him look silly. You always talk of evolution as if it were a single theory, but you know that in fact it's several theories, only parts of which depend on chance. It doesn't deal with the origin of life, but atheists attribute that to chance. It proposes that all forms of life are descended from earlier forms: nothing to do with chance. It proposes that innovations are caused by random mutations: dependent on chance. It proposes that nature ensures that what is useful survives: not chance.
 
If junk is not junk, Dawkins can say that natural selection has ensured the survival of the useful, and that's how non-junk DNA fits in with Darwinism. You say, quite rightly in my view, "complexity is anti-chance", but that does not undermine the natural selection part of the argument. You, Dawkins and I agree that once the mechanism is in place, with all its potential for variation, complexity increases and we have evolution. You and I reject random mutations in favour of intelligence built into the genome, and I agree with you that the almost unfathomable complexity of this mechanism undermines the atheist's faith in origin by chance, and favours origin by design. But as usual that only leads us to the problem of the origin of a designer, which is even more unfathomable. You choose to believe in the unfathomable designer, Dawkins chooses to believe in the chance origin of the unfathomable genome, and I choose not to choose.

Genome complexity: pseudogenes

by David Turell @, Monday, August 26, 2013, 00:18 (3869 days ago) @ dhw

dhw: You always talk of evolution as if it were a single theory, but you know that in fact it's several theories, only parts of which depend on chance. It doesn't deal with the origin of life, but atheists attribute that to chance. It proposes that all forms of life are descended from earlier forms: nothing to do with chance.-Of course chance play a role here. Gould's point about contingency is a counter to your statement. What comes next depends on what came before, and mutations develop forms by a series of accidents. Gould called us a glorious accident!-> dhw: It proposes that innovations are caused by random mutations: dependent on chance. It proposes that nature ensures that what is useful survives: not chance.-Again not true. Natural selection is dependent upon what is presented to it by chance. It chooses from forms that appear by chance. In a way it does mitigate chance, but chance is still the basis.
> 
> dhw: If junk is not junk, Dawkins can say that natural selection has ensured the survival of the useful, and that's how non-junk DNA fits in with Darwinism. You say, quite rightly in my view, "complexity is anti-chance", but that does not undermine the natural selection part of the argument. You, Dawkins and I agree that once the mechanism is in place, with all its potential for variation, complexity increases and we have evolution. -Again be careful. Natural selection has no 'potential for variation', it acts on variation. And as for 'junk' it supports the atheist idea that evoluton is a random walk into the future, purposeless to its core, and junk piled up as garbage might under such circumstances, as a hunt and peck approach to complexity might create.-> dhw: You and I reject random mutations in favour of intelligence built into the genome, and I agree with you that the almost unfathomable complexity of this mechanism undermines the atheist's faith in origin by chance, and favours origin by design. But as usual that only leads us to the problem of the origin of a designer, which is even more unfathomable. You choose to believe in the unfathomable designer, Dawkins chooses to believe in the chance origin of the unfathomable genome, and I choose not to choose.-You don't have to choose. Don't act too surprised when you arrive at the Pearly Gates.

Genome complexity: pseudogenes

by dhw, Monday, August 26, 2013, 15:36 (3868 days ago) @ David Turell

dhw: You always talk of evolution as if it were a single theory, but you know that in fact it's several theories, only parts of which depend on chance. It doesn't deal with the origin of life, but atheists attribute that to chance. It proposes that all forms of life are descended from earlier forms: nothing to do with chance. It proposes that innovations are caused by random mutations: dependent on chance.-DAVID: Of course chance play a role here. Gould's point about contingency is a counter to your statement. What comes next depends on what came before, and mutations develop forms by a series of accidents. Gould called us a glorious accident!
 
The theory that all forms of life are descended from earlier forms (whether you believe it or not) has nothing to do with chance. But Darwinism also proposes that what those forms ARE depends on chance in the form of random mutations. Many theists believe in guided common descent (I thought you were one of them), and not in random mutations. They accept one theory and not the other. Once again you are conflating separate ideas. -DHW: It proposes that nature ensures that what is useful survives: not chance.-DAVID: Again not true. Natural selection is dependent upon what is presented to it by chance. It chooses from forms that appear by chance. In a way it does mitigate chance, but chance is still the basis.-Another conflation. Darwinists believe that chance produces the organs and organisms, and chance dictates changes in the environment. But when one organism survives and another disappears, that is not by chance ... it is the logical outcome of an ability/inability to cope with the environment. You have said yourself that natural selection does not PROVIDE that ability ... it only begins when organs and organisms already exist.-dhw: If junk is not junk, Dawkins can say that natural selection has ensured the survival of the useful, and that's how non-junk DNA fits in with Darwinism. You say, quite rightly in my view, "complexity is anti-chance", but that does not undermine the natural selection part of the argument. You, Dawkins and I agree that once the mechanism is in place, with all its potential for variation, complexity increases and we have evolution.-DAVID: Again be careful. Natural selection has no 'potential for variation', it acts on variation.
 
It is the mechanism of the genome that has the potential for variation.-DAVID: And as for 'junk' it supports the atheist idea that evoluton is a random walk into the future, purposeless to its core, and junk piled up as garbage might under such circumstances, as a hunt and peck approach to complexity might create.-This sentence is difficult to follow. Yes, junk supports the idea of non-design, but an atheist can always switch to the claim that non-junk supports the concept of natural selection (survival of what is useful). In the same way, believers used to think God created species separately, but when the theory of common descent caught on, some of them switched to the idea that God directed evolution. As I keep saying, you can twist information to fit any theory.-dhw: You and I reject random mutations in favour of intelligence built into the genome, and I agree with you that the almost unfathomable complexity of this mechanism undermines the atheist's faith in origin by chance, and favours origin by design. But as usual that only leads us to the problem of the origin of a designer, which is even more unfathomable. You choose to believe in the unfathomable designer, Dawkins chooses to believe in the chance origin of the unfathomable genome, and I choose not to choose.-DAVID: You don't have to choose. Don't act too surprised when you arrive at the Pearly Gates.-They'll never let me in.

Genome complexity: pseudogenes

by David Turell @, Monday, August 26, 2013, 17:19 (3868 days ago) @ dhw


> DAVID: Of course chance play a role here. Gould's point about contingency is a counter to your statement. What comes next depends on what came before, and mutations develop forms by a series of accidents. Gould called us a glorious accident!
> 
> dhw: The theory that all forms of life are descended from earlier forms (whether you believe it or not) has nothing to do with chance. But Darwinism also proposes that what those forms ARE depends on chance in the form of random mutations. -I agree with this but the random chance issue does not define the course of evolution as you point out. If we start with a root we have no idea what the tree or bush will look like in the future. And we do not know if common descent is a natural process, since fossil records of speciation are not found, and only presumptive series of fossils exist, a la' the whales. 
> 
> DHW: It proposes that nature ensures that what is useful survives: not chance.
> 
> DAVID: Again not true. Natural selection is dependent upon what is presented to it by chance. It chooses from forms that appear by chance. In a way it does mitigate chance, but chance is still the basis.
> 
> dhw: Another conflation. Darwinists believe that chance produces the organs and organisms, and chance dictates changes in the environment. But when one organism survives and another disappears, that is not by chance ... it is the logical outcome of an ability/inability to cope with the environment.-I'm not conflating. We agree that either chance or my choice of God's guidance leads up to a new variation and then natural selection as a process takes over.- 
> dhw: It is the mechanism of the genome that has the potential for variation.-Agreed
> 
> dhw: Yes, junk supports the idea of non-design, but an atheist can always switch to the claim that non-junk supports the concept of natural selection (survival of what is useful). .... As I keep saying, you can twist information to fit any theory.-Is twisting reasonable logic? Let's be logical.

Genome complexity: pseudogenes

by dhw, Tuesday, August 27, 2013, 20:33 (3867 days ago) @ David Turell

dhw: The theory that all forms of life are descended from earlier forms (whether you believe it or not) has nothing to do with chance. But Darwinism also proposes that what those forms ARE depends on chance in the form of random mutations.
 
DAVID: I agree with this but the random chance issue does not define the course of evolution as you point out. If we start with a root we have no idea what the tree or bush will look like in the future. [Isn't that randomness?] And we do not know if common descent is a natural process, since fossil records of speciation are not found, and only presumptive series of fossils exist, a la' the whales. [The question is not whether it's a "natural process", but whether the theoretical commonality depends on chance.]-I'm pointing out that evolutionary theory is not a single package but a collection of theories, some of which are chance dependent and some of which are not. It is therefore absurd to claim that non-junk proves that evolution is a "failed paradigm", since it does not in any way invalidate the theories of common descent and natural selection. In my view, it might well argue against the chance origin of the genome, but the origin of the genome is not part of the theory of evolution.
 
DHW: It proposes that nature ensures that what is useful survives: not chance.
DAVID: Again not true. Natural selection is dependent upon what is presented to it by chance. It chooses from forms that appear by chance. In a way it does mitigate chance, but chance is still the basis.
dhw: Another conflation. Darwinists believe that chance produces the organs and organisms, and chance dictates changes in the environment. But when one organism survives and another disappears, that is not by chance ... it is the logical outcome of an ability/inability to cope with the environment.
DAVID: I'm not conflating. We agree that either chance or my choice of God's guidance leads up to a new variation and then natural selection as a process takes over.-So why is it "not true" that the survival or disappearance of organisms by natural selection is not by chance?-dhw: Yes, junk supports the idea of non-design, but an atheist can always switch to the claim that non-junk supports the concept of natural selection (survival of what is useful). .... As I keep saying, you can twist information to fit any theory.-DAVID: Is twisting reasonable logic? Let's be logical.-In all controversial subjects, our information is limited and open to interpretation (if it were not, there would be no dispute). Your logical deduction from life's complexities and from what you see as evolution's guided progress towards humanity is that it was designed, and therefore there must be an eternally conscious designer. The atheist's logical deduction from what he sees as the randomness of the evolutionary bush and of life's history, the manner in which science has traced apparent mysteries to material sources, and the lack of evidence and of any conceivable origin for any sort of eternal intelligence, is that there is no designer and we are the product of chance. Each argument is logical, but each argument depends on how you twist the available information.

Genome complexity: pseudogenes

by David Turell @, Tuesday, August 27, 2013, 22:01 (3867 days ago) @ dhw


> dhw: I'm pointing out that evolutionary theory is not a single package but a collection of theories, some of which are chance dependent and some of which are not. It is therefore absurd to claim that non-junk proves that evolution is a "failed paradigm", since it does not in any way invalidate the theories of common descent and natural selection. -I disagree. A collection of disjointed conjectures. Not Darwin's fault as he was ignorant of so much that we know now. He had no idea of the complexities of the living cell. He looked at breeders and extrapolated to the idea that a long enough in time breed selectioning could make new species. Not proven to any degree. The fossil record does not support his gradualism. Species appear de novo, adapt a little and then disappear. The physical appearance of life forms suggests a related bush of life, but homogous genome studies don't bear that out. Any attempt to present evolution as a natural progressive process falls short of what research is showing. Even the development of the understanding of epigenetics doesn't get us to speciation, only necessary adaptation. Natural selection works at that level. The best adapted survive. And then what? The theory, as a proposal of a natural progressive evolutionary process, doesn't answer. Something is missing, and this is where theoretical proposals fit in. I have mine, you have none. How would you propose to go from single-celled to us?

Genome complexity: pseudogenes

by dhw, Wednesday, August 28, 2013, 17:41 (3866 days ago) @ David Turell

dhw: I'm pointing out that evolutionary theory is not a single package but a collection of theories, some of which are chance dependent and some of which are not. It is therefore absurd to claim that non-junk proves that evolution is a "failed paradigm", since it does not in any way invalidate the theories of common descent and natural selection. -(The numbers in David's response are mine, as I shall answer point by point)
 
DAVID: I disagree. (1) A collection of disjointed conjectures. Not Darwin's fault as he was ignorant of so much that we know now. He had no idea of the complexities of the living cell. He looked at breeders and extrapolated to the idea that a long enough in time breed selectioning could make new species. Not proven to any degree. (2) The fossil record does not support his gradualism. Species appear de novo, adapt a little and then disappear. The physical appearance of life forms suggests a related bush of life, but homogous genome studies don't bear that out. Any attempt to present evolution as a natural progressive process falls short of what research is showing. (3) Even the development of the understanding of epigenetics doesn't get us to speciation, only necessary adaptation. Natural selection works at that level. The best adapted survive. And then what? The theory, as a proposal of a natural progressive evolutionary process, doesn't answer. (4) Something is missing, and this is where theoretical proposals fit in. I have mine, you have none. How would you propose to go from single-celled to us?-Ah, you never cease to surprise me. I thought you were a theistic evolutionist! Let me answer you point by point:-(1) Yes, it is a collection of conjectures ... I call them theories ... but it is far from disjointed. The basis is common descent: all forms of life are descended from earlier forms, right back to the single cell. Once you accept this concept, the next logical step is to ask how it proceeds. Darwin's theory is that it does so by an endless sequence of random mutations. Many of us dispute this, though if we accept common descent, organisms have obviously undergone an endless series of changes. Darwin also believes (2) that these changes proceed gradually by small steps to the complexities we know today. Again you and I dispute this, and we have until now agreed that punctuated equilibrium is a far more likely scenario. Finally, nature ensures that changes which benefit organisms in their respective environments survive, while others disappear (natural selection). This is generally accepted. Nothing disjointed here, but controversy over HOW the changes from which nature selects actually take place. -(3) and (4) You seem suddenly to have forgotten that for several months now we have been discussing the hypothesis of the intelligent cell/genome, which you have accepted on the proviso that it has been designed by God. How does speciation happen, progressing from single-celled to us? Through innovation. How does innovation happen? Through the process of single intelligent cells combining. New combinations of cells combine with other combinations of cells, and each new combination brings forth new forms of life. You have drawn our attention to an article that quoted Lynn Margulis, and earlier today I added the quote I'd missed out yesterday, but I'll repeat just one sentence: "In my description of the origin of the eukaryotic cell via bacterial cell merger, the components fused via symbiogenesis are already "conscious" entities." If you won't listen to me, at least listen to her. That is how I "propose to go from single-celled to us." You are arguing that evolution is a "failed paradigm" because junk is not junk. We have long since agreed to jettison random mutations and gradualism. Evolution does not deal with the origin of the genome. So how does non-junk lead to the failure of common descent and natural selection as an evolutionary paradigm?

Genome complexity: pseudogenes

by David Turell @, Wednesday, August 28, 2013, 18:43 (3866 days ago) @ dhw

David;Something is missing, and this is where theoretical proposals fit in. I have mine, you have none. How would you propose to go from single-celled to us?
> 
> dhw: Ah, you never cease to surprise me. I thought you were a theistic evolutionist!-I am. God created the process of evolution and I suspect that He tweakes it now and then- 
> dhw: (1) Yes, it is a collection of conjectures ... I call them theories ... but it is far from disjointed. The basis is common descent: all forms of life are descended from earlier forms, ... though if we accept common descent, organisms have obviously undergone an endless series of changes. ...we have until now agreed that punctuated equilibrium is a far more likely scenario. Finally, nature ensures that changes which benefit organisms in their respective environments survive, while others disappear (natural selection). This is generally accepted. Nothing disjointed here, but controversy over HOW the changes from which nature selects actually take place.-It is a major controversy. How do those punctuated jumps take place. Epigenetics is a very suggestive way, but it only produces modifications. So again I think God tweakes.- 
> 
> dhw: I'll repeat just one sentence: "In my description of the origin of the eukaryotic cell via bacterial cell merger, the components fused via symbiogenesis are already "conscious" entities." If you won't listen to me, at least listen to her. That is how I "propose to go from single-celled to us." So how does non-junk lead to the failure of common descent and natural selection as an evolutionary paradigm?-My concept is still consciousness pervades the universe through God. The atheists love 'junk' as evidence of failed DNA experiments, illustrating a chance method of evolution without purpose. The more purposeful coordination found in the Genome, the less likely chance was ever present. The newest research supports teleology more and more. ENCODE was a shock to atheists and they have produced article after article to discredit it without success.

Genome complexity: pseudogenes

by dhw, Thursday, August 29, 2013, 13:49 (3865 days ago) @ David Turell

I have attacked the claim that non-junk makes evolution into a "failed paradigm". David claims that evolution is a collection of disjointed conjectures. I have tried to show how these conjectures are interlinked.-Dhw: Nothing disjointed here, but controversy over HOW the changes from which nature selects actually take place.-DAVID: It is a major controversy. How do those punctuated jumps take place. Epigenetics is a very suggestive way, but it only produces modifications. So again I think God tweakes.-The intelligent cell/genome would be sufficient to explain the innovations that drive evolution and cause the "punctuated jumps".
 
Dhw: You are arguing that evolution is a "failed paradigm" because junk is not junk. We have long since agreed to jettison random mutations and gradualism. Evolution does not deal with the origin of the genome. So how does non-junk lead to the failure of common descent and natural selection as an evolutionary paradigm?-DAVID: My concept is still consciousness pervades the universe through God. The atheists love 'junk' as evidence of failed DNA experiments, illustrating a chance method of evolution without purpose. The more purposeful coordination found in the Genome, the less likely chance was ever present. The newest research supports teleology more and more. ENCODE was a shock to atheists and they have produced article after article to discredit it without success.-So how does ENCODE lead to the failure of common descent and natural selection as an evolutionary paradigm? Or do you now agree that it doesn't? As regards teleology, I did respond to that earlier, and I think the point is worth developing. Survival of the individual, propagation of the species, self-improvement, exploration, experimentation etc. may be purposes in themselves at all levels of existence. If Margulis is right, and bacterial cells "as already 'conscious' entities" merged to create the eukaryotic cell, you can extrapolate a whole purposeful pattern of evolution from this one advance, but it does not need to be God-driven. The drive can come from within. And so if there is no such thing as junk DNA, that is because organisms inevitably retain what is useful as they fulfil their own purposes. This may be a blow to atheism, but it is not a blow to evolution, which as you yourself have confirmed is perfectly compatible with belief in God.

Genome complexity: pseudogenes

by David Turell @, Thursday, August 29, 2013, 15:40 (3865 days ago) @ dhw


> dhw:The intelligent cell/genome would be sufficient to explain the innovations that drive evolution and cause the "punctuated jumps".-Your major problem is not being able to explain where the intelligence came from. In the past you have conjured it up. It just magically appears.
> 
> dhw: So how does ENCODE lead to the failure of common descent and natural selection as an evolutionary paradigm? Or do you now agree that it doesn't?-It doesn't because I add God's planning. Common descent and natural selection are taking a battering from findings I have mentioned: orphan genes, orphan proteins, loack of genetic homology in trying to make a bush of life look coherent. CD and NS can't work by chance alone.-> dhw: As regards teleology, I did respond to that earlier, and I think the point is worth developing. Survival of the individual, propagation of the species, self-improvement, exploration, experimentation etc. may be purposes in themselves at all levels of existence. If Margulis is right, and bacterial cells "as already 'conscious' entities" merged to create the eukaryotic cell, you can extrapolate a whole purposeful pattern of evolution from this one advance, but it does not need to be God-driven. The drive can come from within. And so if there is no such thing as junk DNA, that is because organisms inevitably retain what is useful as they fulfil their own purposes. This may be a blow to atheism, but it is not a blow to evolution, which as you yourself have confirmed is perfectly compatible with belief in God.-Your comment is left intact, so I can point out that again you are magically inserting comments like: " the drive can come from within' and "they fulfill their own purposes". Sounds to me a single-celled eukaryote has a little planning brain. Yes, teleology is everywhere you look, and you want that by chance also.

Genome complexity: pseudogenes

by dhw, Friday, August 30, 2013, 15:06 (3864 days ago) @ David Turell

1) dhw:The intelligent cell/genome would be sufficient to explain the innovations that drive evolution and cause the "punctuated jumps".
DAVID: Your major problem is not being able to explain where the intelligence came from. In the past you have conjured it up. It just magically appears.-2) dhw: So how does ENCODE lead to the failure of common descent and natural selection as an evolutionary paradigm? Or do you now agree that it doesn't?
DAVID: It doesn't because I add God's planning. -3) dhw: [...] If Margulis is right, and bacterial cells "as already 'conscious' entities" merged to create the eukaryotic cell, you can extrapolate a whole purposeful pattern of evolution from this one advance, but it does not need to be God-driven. The drive can come from within. And so if there is no such thing as junk DNA, that is because organisms inevitably retain what is useful as they fulfil their own purposes. This may be a blow to atheism, but it is not a blow to evolution, which as you yourself have confirmed is perfectly compatible with belief in God.
DAVID: Your comment is left intact, so I can point out that again you are magically inserting comments like: " the drive can come from within' and "they fulfill their own purposes". Sounds to me a single-celled eukaryote has a little planning brain. Yes, teleology is everywhere you look, and you want that by chance also.-Your own comments are also left intact, because they all quite rightly point to my inability to explain the source of intelligence, of consciousness, of "little planning brains" (Margulis's "conscious entities"). And they point to the same gaping hole in your own fantastic scenario, as follows:-4) DAVID: (under "Quantum zeno effect") God is basically in the quantum realm and is concealed, but as a result he is part of everything and is running everything. 
dhw: Do I detect a certain nebulous quality in the word "basically"? Is God concealed in the quantum particles of my brain, running everything? If so, goodbye to free will. 
DAVID: A certain nebulosity has to appear. God is concealed and cannot be absolutely proven, but God gave us free will.-ALL scenarios have to be nebulous, because NOBODY knows the source of intelligence ... and that includes the source of your God's intelligence. Every argument you level against atheistic reliance on chance or the atheistic version of panpsychism can be levelled against your unknown, unknowable, "concealed" Universal Intelligence. No matter how authoritatively you state where God is, what he does, what he intends, and no matter how definitively you invoke your hollow, philosophical magic formula of "First Cause" (hollow because it can just as easily be unconscious as conscious), the basis of your speculations is no more and no less nebulous than that of other fantasies. No, they cannot be "absolutely proven". Nor can they even be "proven". What I have offered is merely an alternative fantasy to your own. I do not believe or disbelieve either of them. I can only sit on my fence and marvel at how theists and atheists ask each other precisely the same question ("Where did it all come from?"), and then criticize each other for their equally blinkered visions, though they end up with precisely the same answer: "We don't know." Or rather more grandly: "A certain nebulosity has to appear."

Genome complexity: pseudogenes

by David Turell @, Friday, August 30, 2013, 15:39 (3864 days ago) @ dhw

dhw: ALL scenarios have to be nebulous, because NOBODY knows the source of intelligence ... and that includes the source of your God's intelligence. Every argument you level against atheistic reliance on chance or the atheistic version of panpsychism can be levelled against your unknown, unknowable, "concealed" Universal Intelligence....I have merely offered an alternative to your own. I do not believe or disbelieve either. I can only sit on my fence and marvel at how theists and atheists ask each other precisely the same question.-It is your right to maintain your fence position.

Genome complexity: RNA polymerases

by David Turell @, Thursday, October 24, 2013, 15:35 (3809 days ago) @ David Turell

"There are three different RNA polymerases, each of which makes specific types of RNA molecule. For example, RNA polymerase II makes messenger RNA ... the 'middle-man' that carries the information encoded in DNA to a ribosome where it can be used to make a protein. RNA polymerases I and III make parts of the machinery which reads that messenger RNA: I builds the RNA that will eventually form a ribosome, while III makes the transfer RNA that carries the protein building blocks to the ribosome for assembly. Scientists have known for over a decade what RNA polymerase II looks like and how it works, but obtaining detailed information on the structures of its counterparts has proven extremely difficult. Now that they have managed to do so for RNA polymerase I, Müller and colleagues have found explanations for some of the protein's particularities."- Read more at: http://phys.org/news/2013-10-bigger-faster-3d-reveals-protein.html#jCp

Genome complexity: translation control

by David Turell @, Saturday, October 19, 2013, 21:43 (3814 days ago) @ David Turell

Substitute one amino acid and alter function. How did evolution construct this mechanism? An argument from incredulity, because the odds for develping the right choices are so great.-http://darwins-god.blogspot.com/2013/10/regulating-regulators-single-arginine.html-http://darwins-god.blogspot.com/2013/10/failure-how-evolutionists-react.html

Genome complexity:spliceosomes

by David Turell @, Thursday, September 12, 2013, 02:15 (3852 days ago) @ David Turell

Slicing and dicing DNA to create functional gene expressions:-"The spliceosome is truly one of the most remarkable molecular machines in the cell. My purpose here was only to offer readers a small glimpse of this elegant work of nanotechnology, leaving out, of course, much important detail. As I venture deeper and deeper into the hidden world of the cell, the more I am filled with a tremendous sense of awe at the sheer genius and beauty of the design. If such engineering sophistication were encountered in any other realm of inquiry, it would immediately be attributed to intelligence. If biological systems give every appearance of having been designed, are we not justified -- in the absence of a viable alternative explanation -- in inferring that they most likely are the product of design? -- See more at: http://www.evolutionnews.org/2013/09/the_spliceosome_1076371.html#sthash.3SgN8kFB.dpuf

Genome complexity:midbodies

by David Turell @, Wednesday, December 04, 2013, 17:58 (3768 days ago) @ David Turell

What is left when two cells divide is a midbody which goes to one cell only, and we still don't know why, but it makes each cell not really twins, like was thought for ages.-"Regardless of its role in development, there seems to be agreement now among cell biologists that the midbody is important for the cell. Additionally, midbody retention delegitimizes an assumption to which most biologists ascribed for decades: that daughter cells are essentially the same, receiving equal contributions from the parent cell. "When you say that cells are identical when they're divided, it's not true," says Doxsey: the cell that internalizes the midbody carries hundreds of proteins that its sister does not.
 
What exactly this means to the cell, however, remains to be seen. Midbodies "could be completely irrelevant," Mitchison says, "or they could be doing something interesting.' "-
http://www.the-scientist.com//?articles.view/articleNo/38397/title/One-Man-s-Trash---/

Genome complexity:misfolded proteins

by David Turell @, Tuesday, December 10, 2013, 15:24 (3762 days ago) @ David Turell

Proper function by proteins require proper folding. It is not just stringing together amino acids but folding the string into the right configuration:-"A wide range of diseases are caused by an accumulation of misfolded proteins. Among the diseases are neurodegenerative diseases like Alzheimer's disease, Parkinson's disease and Huntington's disease. Other diseases include certain types of diabetes, inherited cataracts and cystic fibrosis."-http://www.sciencedaily.com/releases/2013/12/131209181101.htm

Genome complexity: how little we understand

by David Turell @, Tuesday, December 10, 2013, 15:54 (3762 days ago) @ David Turell

An excellent essay by PZ Myers on how to think about the complexities of genome function:-http://scienceblogs.com/pharyngula/2013/12/07/the-reification-of-the-gene/

Genome complexity: how little we understand

by David Turell @, Tuesday, December 10, 2013, 16:00 (3762 days ago) @ David Turell

An excellent essay by PZ Myers on how to think about the complexities of genome function:
> 
> http://scienceblogs.com/pharyngula/2013/12/07/the-reification-of-the-gene/-Dawkins commentary to the original Dobbs article:-http://www.richarddawkins.net/foundation_articles/2013/12/6/adversarial-journalism-and-the-selfish-gene#

Genome complexity: DNA double coded

by David Turell @, Friday, December 13, 2013, 05:32 (3759 days ago) @ David Turell

There is a code for protein production and a code for transcription control and gene expression:-http://www.sciencemag.org/content/342/6164/1367-All by chance.-"Since the genetic code was deciphered in the 1960s, scientists have assumed that it was used exclusively to write information about proteins. UW scientists were stunned to discover that genomes use the genetic code to write two separate languages. One describes how proteins are made, and the other instructs the cell on how genes are controlled. One language is written on top of the other, which is why the second language remained hidden for so long.
 
"For over 40 years we have assumed that DNA changes affecting the genetic code solely impact how proteins are made," said Stamatoyannopoulos. 'Now we know that this basic assumption about reading the human genome missed half of the picture. These new findings highlight that DNA is an incredibly powerful information storage device, which nature has fully exploited in unexpected ways.' "

Genome complexity: introns and exons

by David Turell @, Saturday, December 21, 2013, 15:35 (3751 days ago) @ David Turell

Exons are used to make protein and introns are an interruptions in the gene itself and must be spliced out. In other words if there were no introns there would not be the need for a complex spiicing mechanism. Therefore it is reasonable to conclude that introns serve some sort of important purpose. A new paper shows that introns do not follow an homologous descent (orthologous is the correct term)every time when gene evolution is studied as evolution progresses.-"The problem is that if the first introns just happened to be randomly inserted into genes for no reason, then there would be no splicing machinery to remove them. And the failure to remove the introns would render the genes useless. This is not to say evolutionists cannot contrive explanations for introns, such as introns initially splicing themselves and the splicing machinery somehow evolving later. But such explanations are circuitous, just-so stories adding tremendous complexity and serendipity to the theory.
 
"Beyond this basic problem, research has also been revealing that introns are not functionless, do not insert randomly in the genome, and do not fall into the common descent pattern. These last two findings were recently reinforced in a new study of a gene known as the eukaryotic translation elongation factor-1a gene."-http://darwins-god.blogspot.com/2013/12/heres-another-study-showing-introns-are.html

Genome complexity: introns and exons

by David Turell @, Friday, December 27, 2013, 02:59 (3745 days ago) @ David Turell

Methylation changes in DNA alter gene production and/or expression. Here is an enzyme that removes methylation to prepare for other epigenetic changes.:-"The finding is important for the field of epigenetics because Tet enzymes chemically modify DNA, changing signposts that tell the cell's machinery "this gene is shut off" into other signs that say "ready for a change."
 
"Tet enzymes' roles have come to light only in the last five years; they are needed for stem cells to maintain their multipotent state, and are involved in early embryonic and brain development and in cancer."-
 Read more at: http://phys.org/news/2013-12-epigenetics-enigma-enzyme-methylation.html#jCp

Genome complexity: RNA repairers

by David Turell @, Wednesday, February 12, 2014, 17:44 (3698 days ago) @ David Turell

RNA seems to be in charge of DNA repair:-http://www.the-scientist.com//?articles.view/articleNo/39137/title/DNA-Damage-Scout/

Genome complexity: epigentic repair

by David Turell @, Monday, February 17, 2014, 17:08 (3693 days ago) @ David Turell

How neurons repair axons:-http://www.the-scientist.com//?articles.view/articleNo/38957/title/Epigenetics-of-Regeneration/

Genome complexity: gene expression controls

by David Turell @, Wednesday, February 26, 2014, 15:30 (3684 days ago) @ David Turell

Good diagram to show the different levels of influence:-http://en.wikipedia.org/wiki/File:Gene_expression_control.png

Genome complexity: transcription initiation

by David Turell @, Friday, March 07, 2014, 01:45 (3676 days ago) @ David Turell

Look at how complex the enzymes are. From E. coli research:-http://sandwalk.blogspot.com/2014/03/the-crystal-structure-of-e-coli-rna.html#more

Genome complexity: new histone code

by David Turell @, Friday, March 14, 2014, 15:45 (3668 days ago) @ David Turell

Add another level of coding, how cells are differentiated into many types; a histone code:--http://phys.org/news/2014-03-unravhttp://phys.orgeling-mystery-histone-code-gene.html

Genome complexity: new histone code

by David Turell @, Friday, March 14, 2014, 17:22 (3668 days ago) @ David Turell

Add another level of coding, how cells are differentiated into many types; a histone code:
> 
> 
> 
Proper site: -http://phys.org/news/2014-03-unraveling-mystery-histone-code-gene.html--"Scientists have discovered a new mechanism that protects active genes from being silenced during cell division. They found that two variants of the same protein can distinguish active and inactive areas of the genome. The two variants differ by just one amino acid, circled here. Researchers captured the atomic structure of the two variants using a kind of molecular photography, shown here. They discovered that the single amino acid change is recognized by an enzyme (in red and blue here) that adds a silencing mark to only one variant (indicated with an arrow), instructing the cell to keep those areas of the genome inactive. Credit: Dr. Robert Martienssen, Cold Spring Harbor Laboratory -"Every cell in our body has exactly the same DNA, yet every cell is different. A cell's identity is determined by the subset of genes that it activates. But how does a cell know which genes to turn off and which to turn on? While the genetic code carried in our DNA provides instructions for cells to manufacture specific proteins, it is a second code that determines which genes are in fact activated in particular cell types.-"This second code is carried by proteins that attach to DNA. The code-carrying proteins are called histones. Today, researchers at Cold Spring Harbor Laboratory (CSHL) and colleagues publish research revealing a new layer of complexity in the histone code. They have found that the slightest variation in a single histone protein can have dramatic effects on how the genes encoded in our DNA are used.
 
"Histones are vitally important because our genetic material is vast: every cell in the body has more than six feet of DNA bundled within a tiny nucleus, a space much smaller than can be seen with the naked eye. For such a massive amount of DNA to be compacted into a microscopic space, it must be wound tightly around spool-like assemblies of proteins. Each of those spools is made up of eight histone proteins. It takes millions of spools in every cell to bundle the entire genome."

Genome complexity: new histone code

by BBella @, Saturday, March 15, 2014, 01:27 (3668 days ago) @ David Turell

More on Epigentics and the Histones:-http://www.metabolics.com/blog/an-international-guide-to-epigenetics/-Just a taste of this very interesting blog:->The study demonstrated that many gene good codes were switched off in the DNA when the DNA was subjected to strong emotions of anger, fear, frustration or stress and were switched back on when subjected to positive emotion again. Dr Joe Dispenza with a background in biochemistry, neurology and cellular biology explains that "bombarding" the cell with the same attitude ( or emotion and the chemicals or neuropeptides released by that emotion ), means that when the cell divides the next cell will have more receptor sites for those particular neuropeptides and less receptor sites for nutrients for vitamins and minerals such as those required for methylation to stop the gene expression.

Genome complexity: new histone code

by David Turell @, Saturday, March 15, 2014, 04:52 (3667 days ago) @ BBella

bbella: More on Epigentics and the Histones:
> 
> http://www.metabolics.com/blog/an-international-guide-to-epigenetics/
... 
> Just a taste of this very interesting blog:
> 
> >The study demonstrated that many gene good codes were switched off in the DNA when the DNA was subjected to strong emotions of anger, fear, frustration or stress and were switched back on when subjected to positive emotion again. Dr Joe Dispenza with a background in biochemistry, neurology and cellular biology explains that "bombarding" the cell with the same attitude ( or emotion and the chemicals or neuropeptides released by that emotion ), means that when the cell divides the next cell will have more receptor sites for those particular neuropeptides and less receptor sites for nutrients for vitamins and minerals such as those required for methylation to stop the gene expression.-Thanks. Great article on histones, and the Nucleasome. Very clear description and of the epgenetic effects on gene expression with methylation and acetylation. It is where I get to the nuitritional supplement part that I cringe a little. Those additives are not that targeted.-On the other hand I follow a Mediterranean diet and swim 21 minutes six days a week against the clock at a sub-maximal exercise pulse, all because of my background training in exercise physiology.

Genome complexity: epigenetic controls

by David Turell @, Thursday, March 20, 2014, 17:06 (3662 days ago) @ David Turell

New mechanisms found:-
"The discovery made by a 12-member all-Indiana University team of scientists led by IU biologist and biochemist Craig Pikaard provides important new insight into how plant cells know to silence a genetic locus—that specific place on a chromosome where a gene is located—in every successive generation.
 
Rather than rely on intrinsic, DNA sequence-based information, the cells instead must recall the need to silence specific loci by relying on chemical marks displayed on the complex of DNA and proteins called chromatin. Addition, or removal, of one-carbon (methyl) or two-carbon (acetyl) chemical tags are ways of modifying chromatin that can impart additional, epigenetic (literally, "above genetic") information to a locus beyond the genetic information encoded in the DNA."-
 Read more at: http://phys.org/news/2014-03-gene-silencing-molecular-memory-tags.html#jCp

Genome complexity: ancient transcription controls

by David Turell @, Friday, March 21, 2014, 00:48 (3662 days ago) @ David Turell

The sea anemone has both animal and plant characteristics in its genome.:-"A team led by evolutionary and developmental biologist Ulrich Technau at the University of Vienna has discovered that sea anemones display a genomic landscape with a complexity of regulatory elements similar to that of fruit flies or other animal model systems. This suggests that this principle of gene regulation is already 600 million years old and dates back to the common ancestor of human, fly and sea anemone. On the other hand, sea anemones are more similar to plants rather to vertebrates or insects in their regulation of gene expression by short regulatory RNAs called microRNAs."-http://www.sciencedaily.com/releases/2014/03/140318113816.htm-Note how ancient this complex mechanism is. Still looks like pre-planning to me.

Genome complexity: gene expression control

by David Turell @, Tuesday, March 25, 2014, 20:09 (3657 days ago) @ David Turell

Bends and turns of DNA control gene expression or supression:-http://www.the-scientist.com//?articles.view/articleNo/39545/title/DNA-Bends-Control-Gene-Activation/

Genome complexity: gene expression control

by David Turell @, Tuesday, April 01, 2014, 16:19 (3650 days ago) @ David Turell

The same protein is used in two different ways by two different bacteria in controlling reactions to stress.:-http://phys.org/news/2014-04-versatility-genetic-aids-rapid-microbial.html

Genome complexity: cell controls

by David Turell @, Friday, April 11, 2014, 15:34 (3640 days ago) @ David Turell

Osmotic pressure controls for cell membranes are finally yielding to discovery. siRNA's are used, a gene is identified:-http://www.the-scientist.com//?articles.view/articleNo/39681/title/Key-Osmotic-Channel-Protein-Identified/

Genome complexity: fighting retrotranspositions

by David Turell @, Sunday, April 27, 2014, 16:02 (3624 days ago) @ David Turell

Some DNA plays a rogue process, contaminating DNA with bad mutations. There is a defense mechanism:-"In addition to fighting LINE-1 jumps that can cause mutations, APOBEC enzymes also fight off certain viruses. In fact, scientists first discovered these enzymes when observing how human cells fight off infection by HIV, the virus that causes AIDS.
 
:Just like HIV, LINE-1 spreads throughout our DNA by making an RNA copy of its genetic sequence. Then, the RNA is copied back into a new LINE 1 copy that can slide into a new location in our DNA -- a process called retrotransposition.
 
"In this new paper, the researchers show that LINE-1 has one important point of vulnerability. When the new DNA copy peels away from the RNA, an APOBEC3A molecule can attach and change some of the "letters" or base-pairs (rungs on the DNA ladder) in the DNA sequence. Specifically, it changes the "C" bases to "U" bases. The presence of those U bases triggers the cell's cleanup mechanism to come in and dismantle the new copy of the rogue DNA.
 
"In other words, APOBEC3A preempts a potential mutation by LINE-1 jumping, by itself causing a mutation in the new LINE-1 copy that the cell then destroys. But APOBEC3A can pose a mutation danger to the rest of our DNA -- which means our cells must strike a balance between a vigorous defense and the danger of friendly fire.
 
"This kind of intracellular "immunity" may have been raging since the beginnings of life on earth, Moran speculates. LINE-1 contains the code for a molecule called reverse transcriptase -- the kind of molecule that would have been crucial when higher life forms started to evolve and use DNA instead of the less stable RNA to carry genetic information." (Love these speculations!)-
http://www.sciencedaily.com/releases/2014/04/140425091846.htm

Genome complexity: de nova or orphan genes

by David Turell @, Tuesday, April 29, 2014, 15:13 (3622 days ago) @ David Turell

Ones that appear with no predecessor, often in junk DNA (non-coding) regions:-http://www.nytimes.com/2014/04/29/science/the-continuing-evolution-of-genes.html?emc=edit_th_20140429&nl=todaysheadlines&nlid=60788861

Genome complexity: enhancer RNA

by David Turell @, Wednesday, May 07, 2014, 19:54 (3614 days ago) @ David Turell

Another way to modigy gene actions:-http://www.the-scientist.com//?articles.view/articleNo/39906/title/Exploring-the-Roles-of-Enhancer-RNAs/

Genome complexity: RNA control of translation

by David Turell @, Tuesday, May 20, 2014, 16:25 (3601 days ago) @ David Turell

Stop an inhibitor:-http://www.the-scientist.com//?articles.view/articleNo/40015/title/RNA-Puts-Proteins-in-a-Headlock/

Genome complexity: Editing

by David Turell @, Tuesday, May 27, 2014, 14:41 (3594 days ago) @ David Turell

Using special enzymes, humans can edit as is done naturally:-These enzymes have been tailored to accurately target a single combination of letters within the three billion base pairs of the DNA molecule. This is the equivalent of correcting a single misspelt word in a 23-volume encyclopaedia.- Read more at: http://phys.org/news/2014-05-breakthrough-dna-genetic-diseases.html#jCp

Genome complexity: Splicosome

by David Turell @, Tuesday, June 03, 2014, 14:47 (3587 days ago) @ David Turell

RNA and 4 proteins make up the splicosome, to edit for protein manufacture. I'm sure Romansh is not incredulous:-http://www.sciencedaily.com/releases/2014/06/140602150707.htm-"The spliceosome is composed of six complexes that work together to edit the raw messages that come from genes, cutting out (hence, splicing) unneeded parts of the message. Ultimately, these messages are translated into proteins, which do the work of cells. The team created crystals of a part of the spliceosome called U6, made of RNA and two proteins, including one called Prp24.
 
"Crystals are packed forms of a structure that allow scientists to capture three-dimensional images of the atoms and molecules within it. The crystals were so complete, and the resolution of the images so high, the scientists were able to see crucial details that otherwise would have been missed.
 
"The team found that in U6, the Prp24 protein and RNA -- like two partners holding hands -- are intimately linked together in a type of molecular symbiosis. The structure yields clues about the relationship and the relative ages of RNA and proteins, once thought to be much wider apart on an evolutionary time scale.
 
"What's so cool is the degree of co-evolution of RNA and protein," Brow says. "It's obvious RNA and protein had to be pretty close friends already to evolve like this." The images revealed that a part of Prp24 dives through a small loop in the U6 RNA, a finding that represents a major milestone on Brow and Butcher's quest to determine how U6's protein and RNA work together. It also confirms other findings Brow has made over the last two decades."

Genome complexity: membrane information

by David Turell @, Thursday, June 05, 2014, 05:28 (3585 days ago) @ David Turell

A review article which defines information in cell membranes, not carried by DNA:-http://bio-complexity.org/ojs/index.php/main/article/viewArticle/BIO-C.2014.2-The embryo is organized not only from DNA instructions but other cellular and structural information

Genome complexity: making DNA

by David Turell @, Saturday, July 19, 2014, 15:27 (3541 days ago) @ David Turell

A fascinating video:-http://www.youtube.com/watch?v=8kK2zwjRV0M&feature=player_embedded

Genome complexity: less junk

by David Turell @, Thursday, July 24, 2014, 18:26 (3536 days ago) @ David Turell

A review of the latest findings. Only 19,000 human genes produce human complexity by other genetic methods:-http://www.evolutionnews.org/2014/07/each_time_genom088091.html

Genome complexity: less junk

by David Turell @, Friday, December 12, 2014, 01:07 (3396 days ago) @ David Turell

DNA folding allows DNA to create multiple functions, through 10,000 loops:-http://phys.org/news/2014-12-scientists-human-loop-ome-revealing-genetic.html-"Folding drives function,"said co-first author Miriam Huntley, a Ph.D. student in the Harvard School of Engineering and Applied Sciences working with Aiden. At the other end of these loops—far away from the genes that they regulate—lay hitherto unknown genetic switches buried deep in so-called junk DNA.-"Our maps of looping revealed thousands of hidden switches that scientists didn't know about before," said Huntley. "In the case of genes that can cause cancer or other diseases, knowing where these switches are is vital."-"The team also discovered a series of rules about how and where loops can form. "If DNA were a shoestring, you could make a loop anywhere. But within the cell, the formation of loops is highly constrained," said Rao. "The loops we see almost all span fewer than 2 million genetic letters; they rarely overlap; and they are almost always associated with a single protein, called CTCF." CTCF is known to be involved in the regulation of the 3D structure of chromatin, the building block of chromosomes.-"The most stunning discovery was about how CTCF proteins form a loop" said Dr. Eric Lander, a corresponding author on the paper. "Even when they are far apart, the CTCF elements that form a loop must be pointing at each other - forming a genomic yin and yang." Lander is director of the Broad Institute, professor of biology at MIT, and professor of systems biology at Harvard Medical School."

Genome complexity: folding DNA

by David Turell @, Saturday, December 13, 2014, 15:01 (3394 days ago) @ David Turell

a video explains how it folds to control gene activation:-https://www.youtube.com/watch?v=dES-ozV65u4

Genome complexity: folding DNA

by David Turell @, Saturday, December 13, 2014, 18:20 (3394 days ago) @ David Turell

I would like a comment on the video on DNA folding. I feel the complexity of the arrangement belies atheism and agnosticism.

Genome complexity: folding DNA

by dhw, Sunday, December 14, 2014, 18:02 (3393 days ago) @ David Turell

DAVID: a video explains how it folds to control gene activation:-https://www.youtube.com/watch?v=dES-ozV65u4-I would like a comment on the video on DNA folding. I feel the complexity of the arrangement belies atheism and agnosticism.-This is clearly going to lead us to our usual dilemma. You and I agree that this complexity cannot be the result of chance. This means that I cannot discount the possible existence of the designer you call God. That is the distinction between the atheist and the agnostic. However, there are alternative explanations which depend on a first cause that is just as inexplicable and irrational as the one you call God. I can only repeat that if you can't explain how first cause energy is so conscious of itself that it can make matter live, reproduce and evolve, how do you expect me to explain how matter can create its own complexities through evolving consciousness? If you go back to the survey, you will see that complexity counts as 10 in its importance, but so do lack of evidence and the illogicality of ALL the basic premises (God, chance, panpsychist evolution).

Genome complexity: folding DNA

by David Turell @, Monday, December 15, 2014, 00:22 (3393 days ago) @ dhw

dhw: You and I agree that this complexity cannot be the result of chance. This means that I cannot discount the possible existence of the designer you call God. That is the distinction between the atheist and the agnostic. However, there are alternative explanations which depend on a first cause that is just as inexplicable and irrational as the one you call God. I can only repeat that if you can't explain how first cause energy is so conscious of itself that it can make matter live, reproduce and evolve, how do you expect me to explain how matter can create its own complexities through evolving consciousness? If you go back to the survey, you will see that complexity counts as 10 in its importance, but so do lack of evidence and the illogicality of ALL the basic premises (God, chance, panpsychist evolution).-And so we have reached different end points. One of the major reasons I believe there has to be a conscious planner at the source of the universe and life is exactly the complexity that you and I agree cannot be the result of chance. I don't see that any of your 'alternative explanations' offer any reasonable solution to the conundrum of 'why is there anything'. I've made my choice. For you everything is illogical. So be it.

Genome complexity: Kangaroos and humans

by David Turell @, Monday, December 29, 2014, 14:27 (3378 days ago) @ David Turell

Genomes look very similar. I think this is more evidence that genomes represent a basic pattern in programming and that other layers of code create the differences:-http://www.reuters.com/article/2008/11/18/us-australia-kangaroos-idUSTRE4AH1P020081118-
"(Reuters) - Australia's kangaroos are genetically similar to humans and may have first evolved in China, Australian researchers said Tuesday.-"Scientists said they had for the first time mapped the genetic code of the Australian marsupials and found much of it was similar to the genome for humans, the government-backed Center of Excellence for Kangaroo Genomics said.-"There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order," center Director Jenny Graves told reporters in Melbourne.-"We thought they'd be completely scrambled, but they're not. There is great chunks of the human genome which is sitting right there in the kangaroo genome," Graves said, according to AAP."

Genome complexity: making immune proteins

by David Turell @, Monday, December 29, 2014, 14:39 (3378 days ago) @ David Turell

Creating antibodies to fight infections is a huge job, as there are so many different pathogens. It involves snipping DNA and recombining it precisely:-"The immune system relies on the formation of specialized proteins (antibodies) that can recognize and immobilize foreign invaders like viruses and bacteria. Since storing individual blueprints for each of these proteins would require huge amounts of DNA, the body instead mixes and matches different chunks of sequence to produce roughly 300 trillion possibilities. This mixing and matching, called recombination, requires that DNA be clipped by the enzyme RAG.-"Recombination is essential for the immune system's ability to recognize and fight new enemies, but too much clipping can cause harmful chromosome rearrangements," says Stephen Desiderio, M.D., Ph.D., director of the Institute for Basic Biomedical Sciences and the senior researcher for the study. "We now know that RAG has a built-in lock that prevents it from getting out of hand as it clips DNA."-"To keep the system efficient, each immune cell makes only a single antibody and only does so after being activated. Several years ago, Desiderio's group found that this level of control is enforced by a segment of RAG called the PHD. The PHD binds to a chemical tag called H3K4me3, which is only found on DNA that is actively being rewritten as RNA. This prevents RAG from recombining DNA that is not active."-
 Read more at: http://phys.org/news/2014-12-mechanism-scissors-dna.html#jCp-Note to dhw: this is how immune cells are sentient and react, by precise molecular action. All evolved by what random process?!

Genome complexity: making immune proteins

by Balance_Maintained @, U.S.A., Monday, December 29, 2014, 17:24 (3378 days ago) @ David Turell


> "The immune system relies on the formation of specialized proteins (antibodies) that can recognize and immobilize foreign invaders like viruses and bacteria. Since storing individual blueprints for each of these proteins would require huge amounts of DNA, the body instead mixes and matches different chunks of sequence to produce roughly 300 trillion possibilities. This mixing and matching, called recombination, requires that DNA be clipped by the enzyme RAG.
> 
>David: Note to dhw: this is how immune cells are sentient and react, by precise molecular action. All evolved by what random process?!-Also note that they are doing precisely what I said they would do if God created the DNA "Program" as a set of functions and routines, mixing and maxing these functions and routines, like common building blocks for specific purposes.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: making immune proteins

by David Turell @, Monday, December 29, 2014, 21:00 (3378 days ago) @ Balance_Maintained


> Tony: Also note that they are doing precisely what I said they would do if God created the DNA "Program" as a set of functions and routines, mixing and maxing these functions and routines, like common building blocks for specific purposes.-As you pointed out, code programs start with basic patterns.

Genome complexity: Kangaroos and humans

by Balance_Maintained @, U.S.A., Monday, December 29, 2014, 15:43 (3378 days ago) @ David Turell

"Kangaroos are hugely informative about what we were like 150 million years ago," Graves said.-
Oh my oh my... now kangaroos are our closest living relative. And here I thought we were most closely related to sponges....

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: Plant DNA discoveries

by David Turell @, Thursday, January 01, 2015, 14:42 (3375 days ago) @ Balance_Maintained

The largest DNAs of all are found here. Horizontal transfer, natural hybridization, high mutation rates, and much more. Interesting read:-http://www.the-scientist.com/?articles.view/articleNo/38729/title/Genomes-Gone-Wild/-"In the last two years, researchers have stumbled upon some “mind-blowing” phenomena in plant genomics, including genomes so strange that “we didn't think [they] could be like that,” says R. Keith Slotkin, a geneticist at Ohio State University. Examples include the peaceful coexistence of two different genomes in a single nucleus and the willy-nilly way plants swap genes among species. And just as with Hooke's, Brown's, and Mendel's fundamental discoveries in plant biology, the bizarre behavior of plant genomes often applies to animals as well."-And the junk issue:-"Two years later, Victor Albert at the University of Buffalo decided to investigate a group of plant cells with nuclei that looked quite different: they appeared to harbor especially tiny genomes. When Albert and colleague Luis Herrera-Estrella sequenced the genome of Utricularia gibba, a bladderwort that forms free-floating mats with hidden underwater bladders that suck in unsuspecting prey, they found that it has one of the smallest genomes ever to be sequenced from a plant—just 82 million base pairs. Even more interesting, the genome is small not because it has fewer genes than other plants. In fact, it has more genes than grapes, papaya, or Arabidopsis. Rather, 97 percent of the plant's genome is protein-coding genes and gene regulatory regions, with only 3 percent having no known function—what scientists often call “junk” DNA.2 That's the complete opposite of the human genome, which is made up of 98 percent junk and 2 percent protein-coding genes.-"“The implications are that you can make a perfectly good complex, multicellular plant with a gigantic genome or a tiny genome,” says Albert. “You probably need approximately the same number of genes, but the ‘junk' or lack of ‘junk' probably doesn't matter much, if it even matters at all.”"

Genome complexity: Plant DNA discoveries

by David Turell @, Thursday, January 01, 2015, 16:08 (3375 days ago) @ David Turell

More on plant research helping to explain how RNA helps to mediate gene functions, so that 20,000 genes can make a human being:-http://phys.org/news/2014-12-scientists-patterns-rna-nuclei.html-"Focusing on sections of RNA that bind to RBPs, [RNA binding proteins] the team found that these sequences have been conserved over evolutionary time and are likely playing an important function in gene regulatory mechanisms.-"The scientists also found a strong inverse relationship between patterns of RBP binding and secondary structure.-"When structure is low, proteins tend to bind those regions and when structure is high, RBPs tend to not bind those regions," Gregory said. "Time and time again, we've seen that the structural context, and not just the RNA sequence, is a selective force in RBP binding."-"Another significant finding was unique patterns of RBP binding and structure present around the start codon of each messenger RNA transcript, which is where a cell's protein-making machinery begins the process of making RNA in proteins.-"This is suggesting that there is a regulatory event happening here even before the RNA comes out of the nucleus and engages with the translation machinery," Gosai said. "It's an exciting place for future studies to start with and figure out what regulation events are happening in the nucleus."-"Two key forms of transcript regulation are alternative splicing, in which pieces of RNA undergo a cut-and-paste process to generate new sequences that can code for various proteins, and alternative polyadenylation, which alters where a transcript ends and an adenine "tail" is added, a process that can enhance either stabilization or degradation of the RNA molecule.-"In their analysis, the Penn biologists found that RBP-binding sites and certain patterns of secondary structure were much more common at sites where alternative splicing and alternative polyadenylation occur.-"In humans, almost 95 percent of genes are alternatively spliced, and the number is at least 60 percent in plants," said Foley. "To see high levels of RBP binding and an interplay with secondary structure at sites of alternative splicing and polyadenylation in plants is good indication of where and how regulation is occurring to produce different proteins from one RNA sequence."- Read more at: http://phys.org/news/2014-12-scientists-patterns-rna-nuclei.html#jCp-
 Read more at: http://phys.org/news/2014-12-scientists-patterns-rna-nuclei.html#jCp

Genome complexity: Making protein without mRNAs

by David Turell @, Friday, January 02, 2015, 21:16 (3374 days ago) @ David Turell

A very new finding. DNA/ mRNA not always needed:-"Yet this study reveals a surprising role for one member of the quality control team, a protein conserved from yeast to man named Rqc2. Before the incomplete protein is recycled, Rqc2 prompts the ribosomes to add just two amino acids (of a total of 20) - alanine and threonine - over and over, and in any order. Think of an auto assembly line that keeps going despite having lost its instructions. It picks up what it can and slaps it on: horn-wheel-wheel-horn-wheel-wheel-wheel-wheel-horn.-"In this case, we have a protein playing a role normally filled by mRNA," says Adam Frost, M.D., Ph.D., assistant professor at University of California, San Francisco (UCSF) and adjunct professor of biochemistry at the University of Utah. He shares senior authorship with Jonathan Weissman, Ph.D., a Howard Hughes Medical Institute investigator at UCSF, and Onn Brandman, Ph.D., at Stanford University. "I love this story because it blurs the lines of what we thought proteins could do."-"Like a half-made car with extra horns and wheels tacked to one end, a truncated protein with an apparently random sequence of alanines and threonines looks strange, and probably doesn't work normally. But the nonsensical sequence likely serves specific purposes. The code could signal that the partial protein must be destroyed, or it could be part of a test to see whether the ribosome is working properly. Evidence suggests that either or both of these processes could be faulty in neurodegenerative diseases such as Alzheimer's, Amyotrophic lateral sclerosis (ALS), or Huntington's."-
 Read more at: http://phys.org/news/2015-01-defying-textbook-science-role-proteins.html#jCp

Genome Complexity; making immune complexes

by David Turell @, Tuesday, January 06, 2015, 23:45 (3370 days ago) @ David Turell

Very complex movements of transposons and other elements (CRISPR) make fresh antibodies against new invaders. This stuff in DNA previously was so-called junk, but isn't:-" Combined with a detailed analysis of the predicted functions of Cas proteins, this discovery led one of us (Koonin) and his team to propose in 2006 that CRISPR-Cas functioned as a form of prokaryotic adaptive immunity, with memory of past infections stored in the genome within the CRISPR “cassettes”—clusters of short direct repeats, interspersed with similar-size nonrepetitive spacers, derived from various MGEs—and to develop a detailed hypothesis about the mechanism of such immunity.-"Subsequent experiments from Philippe Horvath's and Rodolphe Barrangou's groups at Danisco Corporation,along with several other studies that followed in rapid succession, supported this hypothesis. (See “There's CRISPR in Your Yogurt,” here.) It has been shown that CRISPR-Cas indeed functions by incorporating fragments of foreign bacteriophage or plasmid DNA into CRISPR cassettes, then using the transcripts of these unique spacers as guide RNAs to recognize and cleave the genomes of repeat invaders. (See illustration.) A key feature of CRISPR-Cas systems is their ability to transmit extremely efficient, specific immunity across many thousands of generations. Thus, CRISPR-Cas is not only a bona fide adaptive immunity system, but also a genuine machine of Lamarckian evolution, whereby an environmental challenge—a virus or plasmid, in this case—directly causes a specific change in the genome that results in an adaptation that is passed on to subsequent generations. (my bold)-http://www.the-scientist.com/?articles.view/articleNo/41702/title/A-Movable-Defense/

Genome Complexity; mitochondrial proton pump

by David Turell @, Friday, January 09, 2015, 14:50 (3367 days ago) @ David Turell

Pushes protons across the mitochondrial membrane to help defuse free oxygen radicals. We need oxygen but it is very damaging if not controlled. Note how complex the molecule is with its two 'domains'.:-http://www.the-scientist.com//?articles.view/articleNo/41867/title/Mitochondrial-Enzyme-Detailed/-My usual comment. Tell me how Darwinian evolution did this. How much information is required to create it?

Genome Complexity; immunity is Lamarkian

by David Turell @, Tuesday, January 27, 2015, 14:43 (3349 days ago) @ David Turell

In the so-called junk DNA areas many immune battle weapons are formed and used:-http://www.the-scientist.com//?articles.view/articleNo/41702/title/A-Movable-Defense/-"Researchers now recognize that genetic material, once simplified into neat organismal packages, is not limited to individuals or even species. Viruses that pack genetic material into stable infectious particles can incorporate some or all of their genes into their hosts' genomes, allowing remnants of infection to remain even after the viruses themselves have moved on. On a smaller scale, naked genetic elements such as bacterial plasmids and transposons, or jumping genes, often shuttle around and between genomes. It seems that the entire history of life is an incessant game of tug-of-war between such mobile genetic elements (MGEs) and their cellular hosts.-"MGEs pervade the biosphere. In all studied habitats, from the oceans to soil to the human intestine, the number of detectable virus particles, primarily bacteriophages, exceeds the number of cells at least tenfold, and maybe much more. Furthermore, MGEs and their remnants constitute large portions of many organisms' genomes—as much as two-thirds of the human genome and up to 90 percent in plants such as corn.-"Despite their ubiquity and prevalence in diverse genomes, MGEs have traditionally been considered nonfunctional junk DNA.--"The two independent origins of adaptive immune systems in prokaryotes and eukaryotes involving unrelated MGEs show that, in the battle for survival, organisms welcome all useful molecular inventions irrespective of who the original inventor was. Indeed, the origin of CRISPR-Cas systems from prokaryotic casposons and vertebrate V(D)J recombination from Transib transposons might appear paradoxical given that MGEs are primary targets of immune systems. However, considering the omnipresence and diversity of MGEs, it seems likely that even more Lamarckian-type mechanisms have, throughout the history of life, directed genomic changes in the name of host defense.16-"Moreover, the genome-engineering capacity of immune systems provides almost unlimited potential for the development of experimental tools for genome manipulation and other applications. The utility of antibodies as tools for protein detection and of RM enzymes for specific fragmentation of DNA molecules has been central to the progress of biology for decades. Recently, CRISPR-Cas systems have been added to that toolkit as, arguably, the most promising of the new generation of molecular biological methods. It is difficult to predict what opportunities for genome engineering could be hidden within still unknown or poorly characterized defense systems." 

Genome Complexity; handling cell stress

by David Turell @, Wednesday, January 28, 2015, 18:27 (3348 days ago) @ David Turell

There are feedback loop molecules that control stress-related gene changes. These changes revert back to normal when the stress is gone:-
"Stress is unhealthy. The cells use therefore a variety of mechanisms to deal with stress and avert its immediate threat. However, certain stressful situations leave marks that go beyond the immediate response; some even seem to be passed on to the next generation. One school of thought that has gained a lot of attention lately, hypothesizes that the epigenome, chemical modifications on the DNA and on proteins, carries information about external influences such as stress. However, when and how environmental cues trigger changes in the epigenome and thus influence our response has remained largely unknown.-"To investigate how the environment can influence epigenetic processes, FMI Senior group leader Marc Bühler and his group work with fission yeast. In a paper published in Cell Reports, they report the identification of a regulatory circuit that buffers a potentially deleterious epigenetic switch under stressful conditions. The capacity to prevent such an epigenetic change is important to the organism, perhaps because the altered epigenetic state is maintained for many cell divisions, well after the stress has subsided."-
 Read more at: http://phys.org/news/2015-01-cellular-memory-stressful-situations.html#jCp

Genome Complexity; Human Immunity

by David Turell @, Thursday, January 29, 2015, 20:04 (3347 days ago) @ David Turell

Built by immune cells from experiences with infections:-http://www.scientificamerican.com/article/your-immune-system-is-made-not-born/?WT.mc_id=SA_DD_20150129-"In one of the most comprehensive analyses of immune function performed to date, researchers analyzed blood samples from 105 sets of healthy twins. They measured immune cell populations and their chemical messengers—204 parameters in all—before and after participants received a flu shot. Differences in three fourths of these parameters depended less on genetics than on environmental factors, such as diet and prior infections. Genetics had almost no effect on how well individuals responded to the flu vaccine, judged by antibodies produced against the injected material. And among identical twin siblings, who have the same genome, immune system features differed more strikingly within older twin pairs than in younger sets. The findings, published January 15 in Cell, argue that life habits and experiences shape our body's defenses more than the DNA passed down from our parents."-Because of my experience as a family internist, I hardly catch anything now.

Genome Complexity; Histone coding

by David Turell @, Tuesday, February 10, 2015, 19:27 (3335 days ago) @ David Turell

Histones can modify or control genes. There are enzymes that work with histones. the mechanism is complex and very partially understood. DNA is wrapped tightly around histones in a nucleus.:-http://phys.org/news/2015-02-kind-tool-histone-code.html-"One aspect of gene regulation involves enzymes placing chemical tags or modifications on histone proteins - which control a cell's access to the DNA sequences that make up a gene. Properly regulated access allows cells to develop, function, and proliferate normally. The chemical modification of histones is thought to be a form of epigenetic information - information separate from our DNA - that controls gene regulation. This idea is based on the study of the enzymes that chemically modify histones. However, there is a flaw in this argument.-"In complex organisms, such as fruit flies, mice, and humans, scientists have only been able to infer how these enzymes mechanistically accomplish their tasks," said Daniel McKay, PhD, assistant professor of genetics and biology and first author of the paper. "It's been technically impossible to directly study the role of histone modifications. Now, through our collaboration between UNC biologists, we've been able to develop a tool in fruit flies to directly test the function of histones independently of the enzymes that modify them."-"Previously, in mammalian cells, other researchers had discovered that when you mutate a specific modifying enzyme, the result is death because the cells can't replicate.-"With their new fruit fly research model, the UNC researchers altered the histone gene so that this particular enzyme could not modify its histone protein target. The result was not death. In fact, the flies lived and flew as normal flies do. This meant that the enzyme, which was previously proven to be vital to life, must do something else very important.-"There must be another target for that modifying enzyme," Matera said. "There must be another hidden carrier of epigenetic information that we don't know about."-"McKay added, "This is a demonstration of the potential of our epigenetic platform. Going forward, we're going to do a lot more experiments to identify more discrepancies and hopefully other targets of these enzymes. We're on the ground floor of a long-term project."-"This research shows that the epigenetic recipe book for yeast is thin. The recipe book for humans, which is genetically akin to the one for fruit flies, is much thicker, more complex, and full of hidden ingredients scientists have yet to discover.-"Now, scientists have a tool to test the recipes."

Genome Complexity; Histones role

by David Turell @, Tuesday, April 07, 2015, 18:37 (3279 days ago) @ David Turell

They can turn genes on or off:-http://www.sciencedaily.com/releases/2015/04/150402161751.htm -"Scientists studied proteins found in cells, known as histones, which are not part of the genetic code, but act as spools around which DNA is wound. Histones are known to control whether or not genes are switched on.-"Researchers found that naturally occurring changes to these proteins, which affect how they control genes, can be sustained from one generation to the next and so influence which traits are passed on.-"The finding demonstrates for the first time that DNA is not solely responsible for how characteristics are inherited. It paves the way for research into how and when this method of inheritance occurs in nature, and if it is linked to particular traits or health conditions.-"It may also inform research into whether changes to the histone proteins that are caused by environmental conditions -- such as stress or diet -- can influence the function of genes passed on to offspring.-"The research confirms a long-held expectation among scientists that genes could be controlled across generations by such changes. However, it remains to be seen how common the process is, researchers say."

Genome Complexity; T cells alternative splicing

by David Turell @, Tuesday, April 21, 2015, 14:34 (3265 days ago) @ David Turell

T cells fight infection. They are cells stacked in AIDS and HIV. they must make varied responses to each different infection. Alternative splicing of DNA to create different mRNA's accomplishes the feat:-"RNA is both the bridge between DNA and the production of proteins that carry out the functions of life and what guides which and how much protein gets made. As messenger RNA (mRNA) is transcribed from DNA to carry genetic information out of the nucleus, segments that don't code for actual proteins need to be removed from the RNA strand and the remaining pieces spliced together. Different pieces of the expressed gene (exons) are cut out, and these sections are joined together to form the final mRNA strand. Cells gain their ability to produce proteins with various functions by using variations of this splicing.-"The lab of Kristen Lynch, PhD, a professor of in the departments of Biochemistry & Biophysics and Genetics, at the Perelman School of Medicine at the University of Pennsylvania, studies how this splicing occurs in T cells and how it is regulated by multiple proteins. A new study published in the Proceedings of the National Academy of Sciences from her lab describes a cascade of events that may explain changes in gene expression that occur during the development of the human immune system.-"'An understanding of the patterns and mechanisms of alternative splicing is essential for a full comprehension how the genome is interpreted under different conditions to affect protein function," says Lynch.
Alternative splicing is a key mechanism for gene regulation that is regulated in response to developmental and antigen signaling in T cells. However, the extent and mechanisms of regulated splicing, particularly during T-cell development, have not been well characterized. T cells need all kinds of new proteins to go through the necessary alterations to fight infections or mature. The cells do this two ways: turn new genes on to produce new proteins or change how mRNA is spliced together to get different forms of the same proteins. These two mechanisms can work separately or together in a cell"- Read more at: http://phys.org/news/2015-04-messenger-rna-associated-protein-multiple-paths.html#jCp

Genome Complexity; how mitochondria work

by David Turell @, Tuesday, May 05, 2015, 18:21 (3251 days ago) @ David Turell

A complex article describing some of the intricacies of mitochondrial function with complex diagrams:-"Perhaps the more difficult question here is which geometries correspond to which mitochondrial behaviors. The possible behaviors obviously include not just making ATP, but also everything from fatty acid oxidation, to synthesizing steroids, pigments, and other eclectic essentials for the host cell and organism. The possible membrane geometries, much like the various creatively-named models for the generation complex lipid membranes of myelinated nerves, come with descriptive brands like the original 'infolding baffle model' and the more modern 'crista junction' models. Crista junctions are the proteinaceous contacts made a specific critical points between the inner and outer membranes. These various folds transition in various contexts between tubular, lamellar, and helically wound sheets ( particularly common in certain protists).-"A couple of papers from the past week have reported on the roles of some of the more important proteins in shaping membranes. Of note, one published by Polish and German researchers in The Journal of Biological Chemistry found a critical new protein that controls formation of the so-called MICOS system (mitochondrial contact site and cristae organizing system). This protein, Cox17, was already known for its role as a chaperone in the assembly of respiratory complex IV on the inner membrane of mitochondria. Known as cytochrome c oxidase (COX), this is the terminal respiratory complex in the whole chain—the one that hands off the electrons to oxygen. Among other amenities, Cox17 has a series of critical cysteines which appear to involved in recruiting copper to the business end of the mitochondrially encoded COX subunits." -
 Read more at: http://phys.org/news/2015-05-internal-mitochondria.html#jCp

Genome Complexity; Histone coding

by David Turell @, Tuesday, April 11, 2017, 22:05 (2544 days ago) @ David Turell

Found in humans and sea sponges, which are 700 million years old:

https://www.sciencedaily.com/releases/2017/04/170411104532.htm

"University of Queensland School of Biological Sciences researcher Dr Milos Tanurdzic said a collaborative study found sponges use a complex gene regulation toolkit similar to much more complex organisms such as humans.

"Gene regulation refers to how and when a gene is activated.

"'The research implies this complex mechanism was present at the evolutionary dawn of multicellular animals and across animal species as far apart as sponges and humans," Dr Tanurdzic said.

"'Until very recently we thought increasing complexity in the animal kingdom was due to an ever-increasing number of genes that encode information about animal development and growth.

"'However, the genomics explosion of the last decade taught us most animals have a similar number of genes encoded in their DNA. (my bold)

"'The alternative, and today the prevailing explanation, is that gene regulation is responsible for the evolution of animal diversity."

***

"Dr Tanurdzic said a key mechanism responsible for regulating genes in multi-celled organisms was how the DNA was packaged within the genetic material, or genome.

"'DNA associates with special proteins -- called histones -- in the nucleus," he said.

"'Histones can bear certain chemical marks, which in turn determine if the DNA associated with them is going to be turned on or off."

"Histone marking gone awry is also responsible for some of the more insidious genetic errors, such as when a normal cell becomes cancerous.

"'Our study, which used a Great Barrier Reef sponge, Amphimedon queenslandica, set out to discover if this particular mechanism of gene regulation is present in the oldest multicellular animal lineage -- the sponges," he said.

"'Through analysis of DNA with certain histone marks we determined that histone-based gene regulation is part of the sponge gene regulatory tool kit.

"'As the common ancestor of humans and sponges probably lived 700 million years ago, this implies that gene regulatory complexity relying on histone marks was fundamental for the evolution of animal multicellularity and diverse animal forms and functions."

Comment: An excellent example of common descent. Also a demonstration of the layers of control. Note my bold. It's not the number of genes but the layers of controls that make complex animals and plants.

Genome Complexity; Human Immunity

by David Turell @, Friday, July 17, 2015, 16:23 (3178 days ago) @ David Turell

An example of automatic high speed mutations are seen in B cells as the immune system gears up quickly to fight infections by creating antibodies that form a library of defense for the present and the future:-http://www.sciencedaily.com/releases/2015/07/150716160559.htm-"Within germinal centers, B cells evolve in a Darwinian-like fashion. The gene responsible for producing their antibodies mutates rapidly, a million times faster than the normal rate of mutation in the human body, and the cells proliferate. B cells whose mutations increase the antibody's affinity for the antigen are selected, and these cells then continue to mutate and proliferate.-"'Previously, we showed that high affinity cells spend more time dividing and mutating in between rounds of competition. We now show that these high affinity cells also use this additional time more effectively -- by dividing at faster rates," Gitlin says. In this manner, the germinal center produces the high affinity antibodies that are the basis of an effective immune response.-***-"The team's research has focused on the dynamics inside the germinal center. Within it, B cells travel between two areas known as the dark zone and the light zone. In the dark zone, the B cells mutate and proliferate, before traveling to the light zone, where they pick up pieces of antigen. The higher the affinity of their antibodies, the more antigen they pick up.-"Their previous experiments demonstrated that another type of immune cell, the T cell, operates in the light zone to recognize the higher affinity B cells based on the amount of antigen they display. The more antigen the B cells present to T cells, the stronger the signal the T cells send. As a result, the high affinity B cells spend more time in the dark zone in between visits to the light zone.-***-"By labeling DNA replication and following its progression, the team took a close look at how the S phase of the cell cycle, in which the cell copies its DNA in preparation for division, is sped up. They found that acceleration during this phase was due to the double-stranded DNA molecule being unzipped and copied more rapidly at the so-called replication fork.-"'Together, these studies describe two complementary ways in which signals from T cells empower the best equipped set of B cells to take over the immune response during affinity maturation."-Comment: This is the only example I know of that fits dhw's 'inventive mechanism' where cells can mutate at will for a specified purpose.

Genome Complexity; Germ cell enzymes

by David Turell @, Friday, July 17, 2015, 19:08 (3178 days ago) @ David Turell

Two important enzymes in germ cell production are now defined. Note how complex the molecules appear to be. Enzymes are generally huge, and here two work together:-"Co-author of the paper, Anne Ephrussi said: "While we've known Oskar's genetic role in development for some time, we've not known the mechanism by which this takes place. Solving the structure has enabled us to start to see how the different parts of the protein function at a molecular level, which could help us to understand more about this stage of development in a wide range of organisms."-"Using X-ray crystallography, carried out in collaboration with the lab of Christoph Müller, the team was able to determine for the first time the structure of Oskar's two domains, called OSK and LOTUS. The OSK domain is found in some insects, including the fruit fly and the mosquito. The LOTUS domain is more widespread, being found in bacteria, plants and animals, including mice and in humans.-"Using experiments with fruit fly eggs, the team saw that Oskar binds to RNA within the cell - specifically three RNAs derived from genes also known to be important to germline development. But when they looked in more detail, they found that it was only the OSK domain that binds to RNA.-"The LOTUS domain - which they expected to bind to RNA - didn't in fact do so. Instead, the team found that LOTUS binds to an enzyme called Vasa helicase, which is also one of the essential initial ingredients of the germ plasm."- Read more at: http://phys.org/news/2015-07-oskar-revealed.html#jCp

Genome Complexity; spare tire guanines

by David Turell @, Monday, July 20, 2015, 15:01 (3175 days ago) @ David Turell

Apparently guanine can be he most damaged of the base amino acids. DNA carris an extra supply:-http://pubs.acs.org/doi/abs/10.1021/acscentsci.5b00202-From the abstract: "The results support a hypothesis in which regulatory G4s carry a “spare-tire” fifth G-track for aiding in the repair process when these sequences are damaged by radical oxygen species, a feature observed in a large number of these sequences. Furthermore, formation and repair of oxidized bases in promoter regions may constitute an additional example of epigenetic modification, in this case of guanine bases, to regulate gene expression in which the G4 sequences act as sensors of oxidative stress."

Genome Complexity; making immune complexes

by David Turell @, Tuesday, January 19, 2016, 14:56 (2992 days ago) @ David Turell

The regulator of gene control of making antibodies, many of which last a lifetime, has been found:-http://www.sciencedaily.com/releases/2016/01/160118184950.htm-"Plasma cells are white blood cells that develop from B-cells. They are the effector cells of the humoral immune response. Their main function is to produce antibodies that patrol the body in large numbers to neutralize harmful invaders. A functional plasma cell produces up to 10,000 antibodies per second to release them into the blood stream. This outstanding achievement can be visualized with a powerful microscope, as active plasma cells are packed with antibody-producing vesicles, constituting the so-called endoplasmic reticulum that is essential for antibody assembly and secretion.-"B-cells need to be activated by antigens (foreign substances) in order to develop into plasma cells. They first form plasmablasts that migrate to the bone marrow where they survive for many years or even decades. The long-lasting protection provided by active vaccines is based on this immunological memory of plasma cells.-***-"In a five-year project, the team succeeded in deciphering the role of the protein Blimp1 as a central regulator of plasma cell development and function. In its current issue, the science journal Nature Immunology publishes the results of the team in Vienna as well as the work of Australian colleagues that complements the Viennese results.-"In detailed studies, scientists at the IMP identified all genes that are involved in the development of plasma cells in mice. First author Martina Minnich, whose PhD-thesis provided the groundwork for the publication, explains the results: "We found that more than 50 percent of these genes are regulated by Blimp1. Therefore, this factor must be of vital importance for plasma cells. Furthermore, we were able to show for the first time that Blimp1 not only switches genes off but can also switch other genes on. This is an important discovery for the understanding of plasma cell development."-"'Most of the essential functions of plasma cells are controlled by the factor Blimp1," Meinrad Busslinger summarizes the results. "It regulates their mobility and migration to the bone marrow. Blimp1 is also responsible for the enormous increase in size of the endoplasmic reticulum and the strong up-regulation of antibody production in plasma cells. Humoral immunity would not be possible without Blimp1."-"Even though Blimp1 is necessary for the development of plasma cells, mature plasma cells can survive without this factor. However, when Blimp1 is switched off, they become non-functional as they no longer produce antibodies. This unexpected finding is the result of work carried out at the Walter and Eliza Hall Institute (WEHI) in Melbourne, Australia. The study, which is published back-to-back with the Austrian paper, was led by Stephen Nutt, Head of the Division of Molecular Immunology at WEHI. The picture that emerges from the Australian study perfectly complements the results obtained at the IMP."-Comment: How did chance evolution find just the right protein? Structure:-https://www.google.com/imgres?imgurl=http://www.imcb.a-star.edu.sg/newsimages/290609ainside4.jpg&imgrefurl=http://www.imcb.a-star.edu.sg/newsarchive/290609a.php&h=1002&w=604&tbnid=uLrkyX1fsPiQ1M:&docid=x_rRiN8PP2T3GM&ei=UE6eVriNMsfRjAPGsL3YAw&tbm=isch&ved=0ahUKEwi49YL0kLbKAhXHKGMKHUZYDzsQMwgdKAAwAA

Genome Complexity; amazing immune system

by David Turell @, Thursday, January 28, 2016, 14:16 (2983 days ago) @ David Turell

We get some initial immunity from mother's milk at the start of life and then we build up our own antibodies which can last a lifetime, because there are dangerous bugs everywhere all the time:-http://www.evolutionnews.org/2016/01/the_immune_syst_1102547.html-"Rather than having eyes to see with and ears to hear, the cells of the body interact with chemicals and other cells, both foreign and domestic, through the plasma membrane. The surface of the plasma membrane contains thousands of different molecules that relate to its structure and function. Moreover, to detect a specific set of chemicals on the surface of another cell the plasma membrane must have a specific receptor. These receptors consist of protein molecules that contain a specific grouping of chemicals, resulting in a specific, three-dimensional shape that allows them to chemically bind, like Velcro, to the molecule being detected. -"Pathogenic (disease causing) microbes have specific chemicals on their surface that relate to their structure and function, called pathogen-associated molecular patterns (PAMPs). The first responder cells of the innate immune system have specific molecular structures on the plasma membrane that are able to detect these PAMPs, called pattern-recognition receptors (PRRs). It is estimated that the immune cells of the innate system can identify about one thousand different PAMPs. Since these PAMPs only occur on microbes and not on human cells, these specific receptors (PRRs) allow the cells of the innate immune system to identify invading microorganisms as foreign and the ones to be destroyed. -"As noted previously, when target cells, like the ones lining the tubules in the kidney or the muscles surrounding the arterioles, lock on to a specific hormone or neurohormone, this triggers some action. Similarly, when the first responder immune cells of the innate system use their specific receptors (PRRs) to lock on to the specific chemicals on the surface of the invading microbes (PAMPs), they activate. This activation triggers them to identify the enemy, sound the alarm to bring more defenders to the battle, provide strategic information about the invading force, and repel, incapacitate, or kill the intruders. Here's the starting line-up and how they do it.-***-"When mast cells' specific receptors attach to the specific chemicals of an invading microbe, this activates them to release their granules into the surrounding tissue. The granules contain many chemically active molecules, one of which is histamine. -***-"Macrophages (large eaters) are immune cells that are located in all of the tissues and organs of the body. Like mast cells, they activate when their specific receptors attach to specific chemicals on foreign microbes. This triggers them to engulf and literally swallow up the invader. Then, by using specific enzymes, they chemically digest and kill them in a process called phagocytosis (phagein is Greek for "to eat"). -***-" The main job of activated dendritic cells, once their specific receptors have attached to specific chemicals on the surface of the microbe, is to kill it by phagocytosis and process some of its chemicals to provide important information to the cells of the adaptive immune system. Activated dendritic cells also release cytokines that help to improve and regulate the immune response to foreign microbial invasion."-Comment: And this complexity came from chance! Hah!

Genome Complexity; amazing immune system

by David Turell @, Thursday, February 04, 2016, 15:01 (2976 days ago) @ David Turell

Not only are there antibody producing cells which are modified with a memory to take on any return of a previous pathogen, there are literally white cells ( not red) which roam the blood stream to chomp up invading bacteria:-http://www.evolutionnews.org/2016/01/defending_the_b102559.html-"Neutrophils are produced in the bone marrow and with maturation move out into the blood. Neutrophils are usually the first immune cells from the blood to come to the field of battle. They are attracted to the war zone by cytokines, which are chemical messengers released from injured tissue and activated mast cells, macrophages, and dendritic cells. The process by which they move into the field of battle and toward invading microbes is called chemotaxis. This involves using specific receptors on their plasma membrane to move toward areas of increasing concentration of these chemicals. It's similar to how a bloodhound moves towards its prey by sensing the increasing concentration of the scent, or a shark to blood. Moreover, the same cells that send out cytokines to attract neutrophils and other immune cells also release chemicals that cause inflammation. Inflammation allows the neutrophils to squeeze through the narrow openings between the cells that line the capillaries into the tissues so they can seek out and destroy the enemy.-"Once inside the tissues and brought toward the invading microbes by chemotaxis, the neutrophils activate by using specific receptors on their plasma membrane to attach to specific chemicals on the surface of the intruder. The activated neutrophil usually engulfs the microbe in a process called phagocytosis . Once the microbe is inside, the neutrophil releases various chemicals and enzymes to kill and literally digest it. Neutrophils also kill microbes by releasing the chemical contents of their granules into the tissues.-***-"After neutrophils do their job, they usually die and are phagocytosed by macrophages. Dead neutrophils make up most of the cellular content of pus. Finally, like all activated immune cells, neutrophils release cytokines to promote inflammation, attract other immune cells to the battlefield, and increase the metabolism, often causing fever. -***- "That means the body makes about one million neutrophils per second! -Furthermore, to maintain this constant production, support cells in the bone marrow release a cytokine called Granulocyte Colony Stimulating Factor (G-CSF), which attaches to specific G-CSF receptors on the stem cells in the bone marrow, stimulating them to develop into neutrophils. -Finally, in response to infection and inflammation, some immune cells also release G-CSF, which can often result in a doubling or even tripling of the amount of neutrophils. So, although neutrophils cannot multiply on their own (like microbes can), in response to infection and inflammation some immune cells stimulate the bone marrow to increase neutrophil production. This increase makes more defenders available that can be sent to the battlefield. It is by the release of these cytokines that the body not only develops a fever, but also raises the white blood cell count (leukocytosis), the two main tell-tale signs of infection.-***-"Evolutionary biologists seek to explain how life came into being but they pay attention predominantly to how it looks, not how it must work within the laws of nature to survive. They may speculate on how neutrophils and the control mechanisms involved in their production must have come into being by chance and the laws of nature alone. But this doesn't take into account that this system is irreducibly complex, requiring cells that can produce G-CSF and ones that have specific G-CSF receptors, so they can be instructed to become neutrophils, and cytokines to allow neutrophils to leave the bloodstream, and with specific receptors move toward their prey."-Comment: As a physician I went from simply accepting evolution created this to realizing that evolution cannot create this as an unguided chance process!

Genome Complexity; amazing immune system

by David Turell @, Monday, November 21, 2016, 18:24 (2685 days ago) @ David Turell

Another study into how T cells recognize foreign material when surrounded by a welter of 'self' proteins:

http://medicalxpress.com/news/2016-11-immune-receptors-amplify-invader-mini-machines.html

"When a receptor on the surface of a T cell—a sentry of the human immune system—senses a single particle from a harmful intruder, it immediately kicks the cell into action, launching a larger immune response. But exactly how the signal from a single receptor, among thousands on each T cell, can be amplified to affect a whole cell has puzzled immunologists for decades.

"Now, Salk scientists have discovered the key to the amplification of an "invader" signal. The T cell receptor that detects the intruder turns into a mini-machine, activating and releasing copy after copy of a protein called ZAP70.

***

"T cells are central in the adaptive immune response, which is the body's ability to recognize pathogens and respond to them. A single T cell's receptors screen thousands of molecules at any given second, but most of them originate from the body's own proteins and have to be ignored as "self." Researchers have struggled to explain how, in the wake of overwhelming "self" signals, a T cell can detect and respond to one or two "invader" signals.

"Lillemeier's lab studied ZAP70, a protein that associates with T cell receptors and becomes activated when the receptors recognize a foreign molecule. To track the activity and location of ZAP70 molecules, the team tagged them with a fluorescent marker while anchoring each T cell receptor in place. To the group's surprise, ZAP70 molecules were being activated by the T cell receptors and then moving away, spreading throughout the cell.

***

"By churning out ZAP70 and sending it throughout the cell—as opposed to just activating a handful of ZAP70s and keeping them tethered to the T cell receptor—the immune cells can rapidly spread a signal throughout the cell.

"'What we saw is that at the beginning of signaling, you have lots of ZAP70 being released from the T cell receptor to amplify and distribute the signal," says Lillemeier. "But once the signaling is established, the T cell receptor actually adapts and stops releasing so much of ZAP70."

"Questions remain on how the process works, including what the ultimate destinations of the ZAP70 molecules are and how they go on to transmit signals. But the observation, Lillemeier says, is progress toward understanding how T cells identify and react to pathogens.

"'It's really important to understand this process since T cells are at the center of the adaptive immune response," he says. "If the receptors are not controlled well, you're sick; you might either have an autoimmune disease or you can't respond to infections." Being able to make the receptors have a stronger or weaker signal—perhaps by changing how much ZAP70 they activate and release—could help treat these kinds of diseases, he adds." (my bold)

Comment: This is an automatic cellular reaction, no thought involved. The researchers are now looking for the feedback mechanism to control the reaction, a must in all the biochemistry of life. Not by chance.

Genome Complexity; making B cells

by David Turell @, Saturday, February 04, 2017, 01:53 (2611 days ago) @ David Turell

There are two types of B cells in the spleen which make antibodies against infection invaders. Making them from stem cells require specialized enzymatic actions:

https://www.sciencedaily.com/releases/2017/02/170203101550.htm

"...a research team led by professor Bart Lambrecht (VIB-UGent/UZ Gent) demonstrated that mice genetically lacking in Taok3 did not develop MZB cells, and are more susceptible to bacterial infection.

***

"Using an unexpected finding from another project that identified a protein, Taok3, as the trigger for the development of MZB cells, prof. Lambrecht and his team showed that mice without the genetic ability to make Taok3 developed other types of B cells, but not MZB cells. As a result, they were susceptible to pneumococcus infection, a major cause of respiratory illness.

***

"Two types of B cells are formed in the spleen: MZB cells, named so because they are found in an area of the organ called the 'marginal zone', and follicular B cells. However, scientists knew little about the mechanisms governing why early B cells develop into MZB cells versus follicular B cells.

"Hamida Hammad (VIB-UGent): "We had a 'eureka!' moment after discovering that a little-known protein, Taok3, brings a certain proteinase, ADAM10, to the surface of the immature B cell that triggers its development into an MBZ cell. Without that special event, immature B cells can only develop into follicular B cells."

***

"In mouse strains, the team observed in vivo that without Taok3, immature B cells never 'committed' to becoming MZB cells. MZB cells generate antibodies against encapsulated bacteria such as pneumococcus when they enter the bloodstream.

"Hamida Hammad (VIB-UGent): "With an abundance of only follicular B cells, Taok3-free mice are less capable of fighting these types of bacteria effectively.'"

Comment: As with most of these complex arrangements, an enzyme (ADAM10) is required to carry it out. Enzymes are giant molecules which are designed to carry out very specific actions. This mechanism must be developed in one step, as a step by step evolution would not work. Saltation by a brilliant mind, God, is the answer I prefer.

Genome complexity: de novo or orphan genes

by David Turell @, Tuesday, August 25, 2015, 14:02 (3139 days ago) @ David Turell
edited by dhw, Wednesday, August 26, 2015, 08:29

More research and discussion. It seems a genetic tree of life has huge gaps. And they present a chicken-egg problem. How do they get coordinated into the genetic makeup if they just pop up de novo?:-https://www.quantamagazine.org/20150818-a-surprise-source-of-lifes-code/-"For most of the last 40 years, scientists thought that this was the primary way new genes were born — they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.-"Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They're the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.-"The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum — that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis.-***-"Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What's more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.-***-"Yet creating a gene from a random DNA sequence appears as likely as dumping a jar of Scrabble tiles onto the floor and expecting the letters to spell out a coherent sentence. The junk DNA must accumulate mutations that allow it to be read by the cell or converted into RNA, as well as regulatory components that signify when and where the gene should be active. And like a sentence, the gene must have a beginning and an end — short codes that signal its start and end.-"In addition, the RNA or protein produced by the gene must be useful. Newly born genes could prove toxic, producing harmful proteins like those that clump together in the brains of Alzheimer's patients. “Proteins have a strong tendency to misfold and cause havoc,” said Joanna Masel, a biologist at the University of Arizona in Tucson. “It's hard to see how to get a new protein out of random sequence when you expect random sequences to cause so much trouble.” Masel is studying ways that evolution might work around this problem.-***-"Scientists also want to understand how de novo genes get incorporated into the complex network of reactions that drive the cell, a particularly puzzling problem. It's as if a bicycle spontaneously grew a new part and rapidly incorporated it into its machinery, even though the bike was working fine without it. “The question is fascinating but completely unknown,” Begun said. -***-"A human-specific gene called ESRG illustrates this mystery particularly well. Some of the sequence is found in monkeys and other primates. But it is only active in humans, where it is essential for maintaining the earliest embryonic stem cells. And yet monkeys and chimps are perfectly good at making embryonic stem cells without it. “It's a human-specific gene performing a function that must predate the gene, because other organisms have these stem cells as well,” McLysaght said.-“'How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that's the most important question at the moment.'”-Comment: This is why I believe in theistic evolution.

Genome complexity: copying from DNA

by David Turell @, Tuesday, August 25, 2015, 14:24 (3139 days ago) @ David Turell

Remaking machinery constantly to make copies:-http://www.sciencedaily.com/releases/2015/08/150825083923.htm-"This machine is built afresh, moment by moment as it's needed during the copying process. This assembly-de-assembly is vital to accurate and efficient copying.-***-"Our DNA is stored as two strands that are tightly twisted together and joined like a zip. The most important information sits in the middle of this twisted structure, or in the teeth of the zip, where it's protected from harm. To copy this information, the strands need to be temporarily pulled apart. To do this, the cell recruits a large number of proteins and assembles them into a complex copying machine. A key component in the machine is a ring-shaped enzyme, called DNA helicase, which acts a bit like the clasp on a zip that allows you do it up or un-do it. The helicase unzips the DNA by binding to a strand and pulling it through the centre of its ring, but it is not yet known exactly how the helicase binds to the DNA strand.-"It was thought that Cdc6 acts like a tiny motor to place the helicase on top of the strand. Speck and his collaborators have overturned this theory by showing that the helicase can still get into position even when the Cdc6 motor is turned off. However, without active Cdc6, the cell was unable to proceed to the next stage in the copying process -- the machine was jammed. This showed Cdc6 is vital for the machine to function, but it was still not clear exactly what it does.-"The study shows that, once the early stages of copying have begun, the Cdc6 motor is required for removal of the helicase assembly machine. When the researchers inactivated the Cdc6 motor, the machine remained in place for too long."-Comment: How did this complexity develop step by step? I think it had theistic help.

Genome complexity: de novo or orphan genes

by dhw, Wednesday, August 26, 2015, 22:09 (3138 days ago) @ David Turell

DAVID: More research and discussion. It seems a genetic tree of life has huge gaps. And they present a chicken-egg problem. How do they get coordinated into the genetic makeup if they just pop up de novo?:-https://www.quantamagazine.org/20150818-a-surprise-source-of-lifes-code/-QUOTE: “Scientists also want to understand how de novo genes get incorporated into the complex network of reactions that drive the cell, a particularly puzzling problem. It's as if a bicycle spontaneously grew a new part and rapidly incorporated it into its machinery, even though the bike was working fine without it. “The question is fascinating but completely unknown,” Begun said.” -***
QUOTE: “'How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that's the most important question at the moment.'”-David's comment: This is why I believe in theistic evolution.-Many thanks for some very interesting threads, and in particular for this one. For me it raises the whole image of the macrocosm in the microcosm. If new genes can spring from nowhere and incorporate themselves into existing structures, wouldn't this mirror the whole process of innovation that drives evolution? The Cambrian Mystery is solved if new structures can emerge from nowhere.
 
Theistic evolution? Are you going to tell us that God plans every novel gene? Or might it be that God invented a mechanism that comes up autonomously with an infinite number of novelties? Or might it even be that there is no single mind there at all, but billions of little minds within billions of globules of matter coming up with billions of new combinations? Ah, my friend the intelligent cell....

Genome complexity: de novo or orphan genes

by David Turell @, Thursday, August 27, 2015, 14:44 (3137 days ago) @ dhw


> dhw: Many thanks for some very interesting threads, and in particular for this one. For me it raises the whole image of the macrocosm in the microcosm. If new genes can spring from nowhere and incorporate themselves into existing structures, wouldn't this mirror the whole process of innovation that drives evolution? The Cambrian Mystery is solved if new structures can emerge from nowhere.-But your comment does not answer the problem: "Genes from nowhere" are caused by what mechanism? Noting their arrival opens up questions, not answers.
> 
> dhw: Theistic evolution? Are you going to tell us that God plans every novel gene? Or might it be that God invented a mechanism that comes up autonomously with an infinite number of novelties? Or might it even be that there is no single mind there at all, but billions of little minds within billions of globules of matter coming up with billions of new combinations? Ah, my friend the intelligent cell....-Can intelligence grow from no intelligence? If the first life had intelligence where did it come from, abiogenesis? That is a proposed chance happening.

Genome complexity: de novo or orphan genes

by dhw, Thursday, August 27, 2015, 19:43 (3137 days ago) @ David Turell

dhw: Many thanks for some very interesting threads, and in particular for this one. For me it raises the whole image of the macrocosm in the microcosm. If new genes can spring from nowhere and incorporate themselves into existing structures, wouldn't this mirror the whole process of innovation that drives evolution? The Cambrian Mystery is solved if new structures can emerge from nowhere.-DAVID: But your comment does not answer the problem: "Genes from nowhere" are caused by what mechanism? Noting their arrival opens up questions, not answers.
-It does both. It may answer questions about how evolution works. All explanations lead back to an endless chain of causes and effects, but not knowing the cause of something does not invalidate the effect or the subsequent chain of causes and effects. If genes can spring from nowhere, we may have a solution to the Cambrian mystery. The mechanism and its source are different mysteries. 
 
dhw: Theistic evolution? Are you going to tell us that God plans every novel gene? Or might it be that God invented a mechanism that comes up autonomously with an infinite number of novelties? Or might it even be that there is no single mind there at all, but billions of little minds within billions of globules of matter coming up with billions of new combinations? Ah, my friend the intelligent cell....-DAVID: Can intelligence grow from no intelligence? If the first life had intelligence where did it come from, abiogenesis? That is a proposed chance happening.-According to you, intelligence can indeed grow from no intelligence, unless you think God had an intelligent predecessor. No need to go over the “First Cause” cop-out again, as it always ends up with you believing one version of it, and me neither believing nor disbelieving any version.

Genome complexity: de novo or orphan genes

by David Turell @, Thursday, August 27, 2015, 20:40 (3137 days ago) @ dhw

dhw: All explanations lead back to an endless chain of causes and effects, but not knowing the cause of something does not invalidate the effect or the subsequent chain of causes and effects. If genes can spring from nowhere, we may have a solution to the Cambrian mystery. The mechanism and its source are different mysteries.-But nowhere is like nothing: no cause can be found if nothing is there.
> 
> DAVID: Can intelligence grow from no intelligence? If the first life had intelligence where did it come from, abiogenesis? That is a proposed chance happening.
> 
> dhw: According to you, intelligence can indeed grow from no intelligence, unless you think God had an intelligent predecessor. No need to go over the “First Cause” cop-out again, as it always ends up with you believing one version of it, and me neither believing nor disbelieving any version.-Like Einstein who wanted an eternal universe, I propose an eternal initial intelligence.

Genome complexity: de novo or orphan genes

by dhw, Friday, August 28, 2015, 18:39 (3136 days ago) @ David Turell

dhw: All explanations lead back to an endless chain of causes and effects, but not knowing the cause of something does not invalidate the effect or the subsequent chain of causes and effects. If genes can spring from nowhere, we may have a solution to the Cambrian mystery. The mechanism and its source are different mysteries. -DAVID: But nowhere is like nothing: no cause can be found if nothing is there.
-I take "from nowhere" to mean that we don't know the cause - not that there isn't a cause. If the cell can produce novelties, the cause of its ability to produce them may be some internal, inventive mechanism that we haven't discovered yet. If you think it's some divine computer programme, that hasn't been discovered either. 
 
DAVID: Can intelligence grow from no intelligence? If the first life had intelligence where did it come from, abiogenesis? That is a proposed chance happening.
 
dhw: According to you, intelligence can indeed grow from no intelligence, unless you think God had an intelligent predecessor. No need to go over the “First Cause” cop-out again, as it always ends up with you believing one version of it, and me neither believing nor disbelieving any version. -DAVID: Like Einstein who wanted an eternal universe, I propose an eternal initial intelligence.-I don't think your proposal of an eternal intelligence is anything like the proposal of an eternal universe. However, I'm impressed by the morale-raising implications of your comparison. Like Shakespeare, I write plays.:-D

Genome complexity: de novo or orphan genes

by David Turell @, Friday, August 28, 2015, 22:25 (3136 days ago) @ dhw


> dhw: I take "from nowhere" to mean that we don't know the cause - not that there isn't a cause. If the cell can produce novelties, the cause of its ability to produce them may be some internal, inventive mechanism that we haven't discovered yet. If you think it's some divine computer programme, that hasn't been discovered either.-We both accept that we still don't know how novel speciation occurs.
> 
> DAVID: Like Einstein who wanted an eternal universe, I propose an eternal initial intelligence.
> 
> dhw: I don't think your proposal of an eternal intelligence is anything like the proposal of an eternal universe. However, I'm impressed by the morale-raising implications of your comparison. Like Shakespeare, I write plays.:-D-There had to be an eternal something at the beginning or there would be nothing at all now.

Genome complexity: de novo or orphan genes

by dhw, Saturday, August 29, 2015, 08:31 (3135 days ago) @ David Turell

DAVID: Like Einstein who wanted an eternal universe, I propose an eternal initial intelligence.-dhw: I don't think your proposal of an eternal intelligence is anything like the proposal of an eternal universe. However, I'm impressed by the morale-raising implications of your comparison. Like Shakespeare, I write plays.:-D
 
DAVID: There had to be an eternal something at the beginning or there would be nothing at all now.-Agreed. Energy and matter. A theistic version: the energy is an eternal intelligence. An atheistic version: intelligence evolved out of matter (at some time after the Big Bang, if it happened). Agnostic version: yeah, well, one or the other, with possible variations.

Genome complexity: de novo or orphan genes

by David Turell @, Saturday, August 29, 2015, 14:14 (3135 days ago) @ dhw


> DAVID: There had to be an eternal something at the beginning or there would be nothing at all now.
> 
> dhw: Agreed. Energy and matter. A theistic version: the energy is an eternal intelligence. An atheistic version: intelligence evolved out of matter (at some time after the Big Bang, if it happened). Agnostic version: yeah, well, one or the other, with possible variations.-To me the choice is so clear.

Genome complexity: de novo or orphan genes

by dhw, Sunday, August 30, 2015, 21:28 (3134 days ago) @ David Turell

DAVID: There had to be an eternal something at the beginning or there would be nothing at all now.-dhw: Agreed. Energy and matter. A theistic version: the energy is an eternal intelligence. An atheistic version: intelligence evolved out of matter (at some time after the Big Bang, if it happened). Agnostic version: yeah, well, one or the other, with possible variations.-DAVID: To me the choice is so clear.-That's faith for you.

Genome complexity: how to repair DNA

by David Turell @, Tuesday, September 01, 2015, 15:14 (3132 days ago) @ dhw

A protein is identified that move broken strands to a repair site:-http://www.biotechniques.com/news/biotechniquesNews/biotechniques-360132.html-"In the new study, Mekhail's group induced double-strand breaks either near the telomeric regions, which affect the lifespan of cells and are implicated in cancer, or more internally. Cells carrying the kinesin-14 complex survived by activating the repair pathway while many mutant cells missing the complex died. -"Durocher's team tracked the damaged DNA in living cells using time-lapse microscopy and showed broken DNA moving toward the nuclear envelope. Kinesin-14 was necessary for this process. -"The scientists also introduced a DNA “zip code” sequence adjacent to the double-strand break sites that targeted those spots to Nup84 (i..e., the hospital). This led to a drastic boost in repair, but interestingly, the zip code did not rescue repair entirely. -"It's still unclear exactly how kinesin-14 cooperates with microtubules to shuttle broken DNA to Nup84, but another recent study in yeast showed that certain molecular complexes including another nuclear envelope protein link DSBs to microtubules and are important for repair." -Comment: The complexity of the cell protein mechanisms highly suggests design.

Genome complexity: how to repair DNA

by David Turell @, Thursday, September 03, 2015, 18:01 (3130 days ago) @ David Turell

Another study looks at the complex arrangements of enzymes that helps manage DNA repair:-http://phys.org/news/2015-09-decodes-protein-complex-dna.html-"One enzyme in particular, BRCC36, removes a specific type of ubiquitin that is central to DNA damage repair as well as inflammatory responses. But BRCC36 doesn't act on its own—it functions as part of a complex comprised of several other proteins, one of which is KIAA0157. But how these two work together has remained unclear. Now, thanks to work performed in collaboration between researchers at the Perelman School of Medicine at the University of Pennsylvania and the Lunenfeld-Tanenbaum Research Institute in Toronto, the mechanism is coming into focus.-***-"They found that BRCC36 and KIAA0157 are structurally related proteins, but while the BRCC36 is capable of removing ubiquitin (generally called a DUB for its deubiquitinating function), KIAA0157, is not quite up for that job since it does not bind the metal ions necessary for removing ubiquitin, so is referred to as a "pseudo-DUB."-"By comparing high-resolution structures of two complexes - one containing both a DUB and a pseudo-DUB, and two copies of an inactive DUB by itself—the team determined that KIAA0157 alters the shape of the BRCC36 active site, by swinging an amino acid into position to make the complex able to catalyze chemical reactions.-"They also found that the complete, functional complex contains two BRCC36-KIAA0157 molecule pairs, a symmetrical configuration the authors call a "super-dimer."-***-"According to Greenberg, BRCC36-KIAA0157 is just one of many deubiquitinating enzyme complexes present in cells of complex organisms: "It turns out to be a general mechanism of how this class of deubiquitinating enzymes works." Given the similarity of these related proteins to one another, knowing the structure and mechanism of BRCC36-KIAA0157 should enable researchers to better model the structures of related complexes, and also probe their mechanisms."

Genome complexity: We don't know how DNA works

by David Turell @, Friday, September 04, 2015, 22:29 (3129 days ago) @ David Turell

How do we get a 3-D organism from the 1-D code. We basically don't know:-http://www.huffingtonpost.com/suzan-mazur/neuroscientist-david-edel_b_8051746.html-David Edelman: "One of the problems, and we're still confronting these problems in modern genetics, is that we do not have the ability to discern from a 1D code, which is basically what a given genome is, a 3D organism. We don't yet have any way to explain how 3D organismal form comes about.-*** -"There's an intellectual crisis in modern biology. A hyper-determinist streak runs through the thinking, particularly in molecular biology and genetics. Even if researchers can't get directly from DNA code to a 3D organism, they believe essentially that it's simply a coding problem.-"It's actually more complex. The problem is that we cannot observe a lot of processes in sufficient detail and at all the necessary levels of interaction -- either during individual development or across evolutionary time. And these processes are messier than we believe. Right now, we can't infer processes in a systematic way regarding the relevant levels of morphological change. We don't have the capacity to do that yet. -***-"One of the unfortunate aspects of Western science is that it's hyper-reductionist. There's nothing wrong with that to a certain extent. You can certainly pull things apart to study them and look at the constituent elements; at a certain level of organization they look like a highly mechanical system and to some extent you can discern from your dissections what each element does. When you look at certain molecular biological problems, for example, that's what you see. But the critical issue is that we're talking about much larger systems, systems nested within other systems. It's the interactions across those different levels of organization that need to also be considered.-***-"I also think it's in the nature of trained Western scientists to look for a big breakthrough answer. We scientists tend to admire the mechanistic reduction of classical physics. What my dad used to call a case of "physics envy." We'd love the biological world to cooperate in the same way that the atom and everything else scaled up to the atom behaved prior to Einstein, prior to 20th century physics. For the world to be reducible in a very mechanistic way. I am leery of this conception because biology defies it at every turn."-Comment: I'm told I believe in a god-of-the-gaps by atheists who are offended and comment on my book. Not really. I believe in the complexity of life, way beyond what Darwin imagined. Darwin is the god of atheism, even if he was himself agnostic. What I believe in is that the complexity of life requires God as designer.

Genome complexity: how to repair DNA

by David Turell @, Tuesday, September 08, 2015, 19:54 (3125 days ago) @ David Turell

A different method of DNA repair using another guiding molecule:-http://www.sciencedaily.com/releases/2015/09/150908144143.htm-"Immediately after DNA damage occurs, H2AX gets a mark--it becomes tagged with a chemical moiety known as a phosphate. This process, called phosphorylation, occurs at sites of broken DNA as a way to mediate interactions between key proteins. In the study, the researchers wanted to learn more about how phosphorylation of H2AX helps mediate DNA repair.-***-"This technique enabled the researchers to identify not just the proteins that were known to strongly bind to H2AX and facilitate DNA repair, but also those that were considered "weak binders" as well, says Kleiner.-"Indeed, they found that part of a DNA repair protein known as 53BP1 fits over the phosphorylated part of H2AX "like a glove," says Kleiner. This interaction helps bring 53BP1 to the site of DNA damage, where it mediates the repair of double-stranded breaks in DNA by encouraging the repair machinery to glue the two ends back together.-"'We've identified a component of the DNA repair process that others had previously missed," notes Kleiner. "Scientists have known about 53BP1 for a long time, but didn't understand the function of this particular portion of the protein that interacts with the phosphorylation mark of H2AX. These findings help solve that mystery.'"-Comment: this is obviously intelligently constructed activity follow commands in the cell to protect original DNA coding.

Genome complexity: transcription mechanism

by David Turell @, Tuesday, September 15, 2015, 16:45 (3118 days ago) @ David Turell

How the molecules work together:-http://phys.org/news/2015-09-chemists-physicists-rna-polymerase-real.html-"RNA polymerase II (pol II) plays the key role of transcribing genetic code from DNA into segments of RNA, which pass those instructions on to the molecular machinery that assemble proteins. In order to do this, pol II needs the help of other molecules to form a multi-protein assembly called the preinitiation complex (PIC), which can pry apart the DNA's double-stranded helix and begin the process. As the PIC attaches to a section of DNA, it unwinds the helix and separates the two strands, forming a sort of "bubble" for the enzyme to sneak in and commence its work.-***-"The project was made possible by what Block, the senior author, describes as a "tour de force" of biochemistry from study co-author Kenji Murakami, a former postdoc in Roger Kornberg's lab at Stanford School of Medicine, to build a PIC. Working at Stanford with Kornberg, Murakami, now at the University of Pennsylvania, expressed and assembled 32 different proteins from yeast into the exact molecular machine that is required in higher organisms.-"'What he built is fully functional, and together, we got it to work in my lab at the single-molecule level, which is the first time it has even been attempted with an assembly this complex," Block said. "Even without everything else we learned during this work, this is a significant technical breakthrough."-"Next, they loaded the handmade PIC and a section of template DNA into a custom-built apparatus called an optical trap, in which two powerful lasers essentially hold on to either end of the genetic material. As the PIC initiated pol II activity and began to transcribe the template DNA, it either pulled or pushed the strands of DNA, and this motion affected the light scattered from a third laser in the apparatus. This tiny change in light scattering allowed the researchers to measure the motions of the PIC all the way down to the nanometer level.-***-"The sensitivity of their apparatus allowed the researchers not only to measure the size of the bubble created by the PIC but also to observe the activity of a separate transcription factor, called TFIIH, that serves as the molecular motor to help push the PIC along at the start. -"The researchers were pleased to see the motor in action, as it hadn't been documented before, but it was the size of the transcription bubble - the loop of DNA created to allow the gene to be converted to DNA - that was particularly exciting. Although scientists had seen a similar bubble in bacteria, the version they observed in higher organisms was enormous, at over 10 times larger."-Comment: Note that bacteria have a comparable mechanism. We should assume that cells in a multicellular animal work automatically, and I feel the same is true in bacteria, since the same mechanisms are at work.

Genome complexity: challenges naturalism

by David Turell @, Saturday, September 19, 2015, 21:21 (3114 days ago) @ David Turell

As I wrote in 1992 in my book (two years before my first book was published) the discoveries of increasingly complex mechanisms to create and sustain life would eventually bring an end to the acceptance of Darwin's theory of evolution. This article encapsulates my thinking perfectly:-http://www.evolutionnews.org/2015/07/evolutions_gran097591.html-Evolutionary biology was very much like other sciences up until the 1950s, when the information-bearing capabilities of DNA and RNA were discovered inside living cells.-These discoveries fundamentally changed biology. And as the information payload is increasingly unraveled, we're seeing ever more complex and interdependent assembly instructions, activation circuits, programming sequences, and message payloads. This information is decoded and operated on by molecular machines of similar complexity, and the whole (information + machines) is self-generating, self-sustaining, and self-replicating.-***-Aside from the obvious (and intriguing) challenge of understanding the enormous complexity of life's information payload, evolution purports to explain its origins.-The origin of life is perhaps the most obvious example of information's formidable hurdle to evolutionary explanations. First life requires all of the following:-•Sufficient complex programs and sequencing to support first life's complete lifecycle (i.e., the directions have to be complete and correct).
•Sufficient machinery to interpret the programs and to operate life (i.e., the directions must have proper effect).
•Sufficient programs and machinery to replicate both the programs and the machinery (i.e., the directions must be passed to the next generation).-And all this must be present at the same time, in the same place, in at least one instant in history, at which point the whole must somehow be animated to create life. And all this must occur, by definition, before an organism can reproduce. Without reproduction, there is no possibility to accumulate function, from simple to complex, as required by evolution. Hence, the programs must have contained all the complexity required for first life at inception.-***-So materialists face growing dissonance between their philosophical commitment and biology's complex programming. As the quality and quantity of the discovered interdependent programs and processing machinery increases, the plausibility of material causation gets weaker. So the materialist position is weak, and going in the wrong direction (from their perspective).-On the other hand, for anyone not fully committed to materialist philosophy the options are much more interesting. For those willing to consider the second class of causal force, things begin to fall into place and the dissonance dissipates.-For theists, the second class of causal force is not only acceptable, but expected. Further, theists are unsurprised to learn that the causal forces in class #1 are finely tuned to enable life, and they have no problem with the notion that random events are more likely to destroy information than create it (e.g., there are far more possible non-functioning programs than functioning programs).-Ongoing discoveries about the nature of the information at the core of life present a growing hurdle for the materialist worldview, but are increasingly friendly to any worldview that's open to a pre-biological intelligence with some means to assemble the programs and machinery minimally required for first life.-***
And this is evolution's grand challenge: The complex programs and amazing molecular machines at the heart of life simply cannot be explained by any current or proposed theory of evolution, nor by any other completely material cause. Apologists for materialism cannot hide this fact much longer. Neither the volume of their arguments nor any level of vitriol can change the fact that the data is skewing against them.-Rarely has any field of science had to deal with questions so difficult, or that cut so deeply into the worldviews, minds, and hearts, of thoughtful men and women.-Comment: Not by chance!!!

Genome complexity: challenges naturalism

by dhw, Sunday, September 20, 2015, 14:59 (3113 days ago) @ David Turell

DAVID: As I wrote in 1992 in my book (two years before my first book was published) the discoveries of increasingly complex mechanisms to create and sustain life would eventually bring an end to the acceptance of Darwin's theory of evolution. This article encapsulates my thinking perfectly:-http://www.evolutionnews.org/2015/07/evolutions_gran097591.html-QUOTE: "Aside from the obvious (and intriguing) challenge of understanding the enormous complexity of life's information payload, evolution purports to explain its origins."-No it doesn't. Darwin's theory attempts to explain how different forms of life evolved from earlier forms of life. Your author clearly hasn't read Darwin's book but has seized on the fact that atheists like to conflate the theory of evolution with the theory of abiogenesis. They are not connected. Modern discoveries may well have put paid to Darwin's concept of how the process works, but that does not put paid to the theory of evolution.
 
Here for the umpteenth time is part of Darwin's conclusion in my edition of Origin (not a first edition): “There is grandeur in this view of life, with its several powers, having been originally breathed by the Creator into a few forms of life or one.” David, you have accepted common descent, and that is the bedrock of Darwin's theory. If you agree with his above conclusion, then stop claiming that the theory is nearing the end of acceptance.

Genome complexity: challenges naturalism

by David Turell @, Sunday, September 20, 2015, 18:28 (3113 days ago) @ dhw

dhw: They are not connected. Modern discoveries may well have put paid to Darwin's concept of how the process works, but that does not put paid to the theory of evolution.
> 
> .... David, you have accepted common descent, and that is the bedrock of Darwin's theory. If you agree with his above conclusion, then stop claiming that the theory is nearing the end of acceptance.-You miss the point entirely. The origin of life and the evolution of life are a continuity, totally., and intimately related. First life had to be prepared for the process of evolution which followed in a totally continuous fashion.-You persist in forgetting that I believe in guided evolution. I have not accepted Darwin's theory of how it works. The bedrock of his theory is natural selection which allows for a chance method for evolution and removes the need for guidance. His theory is at its heart passive and purposeless. I thought I've made that clear over and over.

Genome complexity: challenges naturalism

by dhw, Monday, September 21, 2015, 19:55 (3112 days ago) @ David Turell

I shall juxtapose sections of our exchange to bring out the continuity of the argument.-DAVID: As I wrote in 1992 in my book (two years before my first book was published) the discoveries of increasingly complex mechanisms to create and sustain life would eventually bring an end to the acceptance of Darwin's theory of evolution. This article encapsulates my thinking perfectly:http://www.evolutionnews.org/2015/07/evolutions_gran097591.html
QUOTE: “Aside from the obvious (and intriguing) challenge of understanding the enormous complexity of life's information payload, evolution purports to explain its origins.”
Dhw: No it doesn't. Darwin's theory attempts to explain how different forms of life evolved from earlier forms of life. Your author clearly hasn't read Darwin's book but has seized on the fact that atheists like to conflate the theory of evolution with the theory of abiogenesis. They are not connected. -DAVID: You miss the point entirely. The origin of life and the evolution of life are a continuity, totally, and intimately related. First life had to be prepared for the process of evolution which followed in a totally continuous fashion.-But Darwin's theory of evolution does not deal with the origin of life. It leaves that question open. However, if “the Creator” breathed life “into a few forms of life or one”, doesn't that meet your theistic requirements?
 
Dhw: Modern discoveries may well have put paid to Darwin's concept of how the process works, but that does not put paid to the theory of evolution. (My bold)-DAVID: You persist in forgetting that I believe in guided evolution. I have not accepted Darwin's theory of how it works. (My bold)-Neither of us has accepted Darwin's theory of how it works, but that does not mean an end to the acceptance of the whole theory of evolution. It means an end to acceptance of random mutations and gradualism, which we long ago agreed on. I can never forget that you believe in guided evolution, though I wonder how many of your fellow evolutionists, geneticists and biologists believe that your God guided it.-dhw: David, you have accepted common descent, and that is the bedrock of Darwin's theory. If you do not disagree with the above conclusion, then stop claiming that the theory is nearing the end of acceptance.-DAVID: The bedrock of his theory is natural selection which allows for a chance method for evolution and removes the need for guidance. His theory is at its heart passive and purposeless. I thought I've made that clear over and over.-You have. However, in Darwin's book, despite its misleading title, it is not natural selection that produces species but random mutations, which survive or perish according to non-creative natural selection. This, however, relates to the way evolution works, not to the theory that all forms of life - apart from the first - have evolved from earlier forms. (“Evolution: the process by which living organisms have developed from earlier ancestral forms” - Penguin Dictionary of Science.) If you accept that, you accept the theory of evolution, as opposed to that of separate creation.

Genome complexity: challenges naturalism

by David Turell @, Monday, September 21, 2015, 20:25 (3112 days ago) @ dhw


> DAVID: You miss the point entirely. The origin of life and the evolution of life are a continuity, totally, and intimately related. First life had to be prepared for the process of evolution which followed in a totally continuous fashion.
> 
> dhw: But Darwin's theory of evolution does not deal with the origin of life. It leaves that question open. However, if “the Creator” breathed life “into a few forms of life or one”, doesn't that meet your theistic requirements?-To repeat: I know Darwin's theory starts after life arrives, but first life is a continuum with what came next. First life is intimately related to the process of evolution, as the article shows it must contain the preparation for what ever evolved next. I'm discarding Darwin's theory as to the method of evolution, and this article points out one of the strongest reasons I have reached my point of view.-> dhw: However, in Darwin's book, despite its misleading title, it is not natural selection that produces species but random mutations,-I know that.-> dhw:(“Evolution: the process by which living organisms have developed from earlier ancestral forms” - Penguin Dictionary of Science.) If you accept that, you accept the theory of evolution, as opposed to that of separate creation.-I accept evolution. I have my own theory as to how it works.

Genome complexity: challenges naturalism

by dhw, Tuesday, September 22, 2015, 12:19 (3111 days ago) @ David Turell

“Natural selection explains not only the whole of life.....” (Dawkins, The God Delusion.)-When you read that, don't you shake your head in disbelief? The whole of life? (You will also shake your head at the rest of the sentence: “...it also raises our consciousness to the power of science to explain how organized complexity can emerge from simple beginnings without any deliberate guidance.”-(D. Turell 19 Sept.): [I wrote that] “the discoveries of increasingly complex mechanisms to create and sustain life would eventually bring an end to the acceptance of Darwin's theory of evolution.” -I shook my head in disbelief. The whole theory? An end to acceptance of common descent? Back to Creationism? But now compare that to the following statements:-(D. Turell, 21 September): “I'm discarding Darwin's theory as to the method of evolution.” “I accept evolution. I have my own theory as to how it works.” -Ah! That's more like it. Thank you. I would hate to have to label you as a theistic Dawkins. Here is another statement:-QUOTE: “Aside from the obvious (and intriguing) challenge of understanding the enormous complexity of life's information payload, evolution purports to explain its origins.”-I accept all your arguments about continuity etc. but your author here is also doing precisely the same as Dawkins: offering a gross misrepresentation in order to make his case sound more convincing. The theory of evolution does not purport to explain life's origins. We stalwarts of the AgnosticWeb - regardless of beliefs, disbeliefs and non-beliefs - will go on shaking our heads at all such distortions, won't we?

Genome complexity: challenges naturalism

by David Turell @, Tuesday, September 22, 2015, 17:13 (3111 days ago) @ dhw

dhw: QUOTE: “Aside from the obvious (and intriguing) challenge of understanding the enormous complexity of life's information payload, evolution purports to explain its origins.”
> 
> I accept all your arguments about continuity etc. but your author here is also doing precisely the same as Dawkins: offering a gross misrepresentation in order to make his case sound more convincing. The theory of evolution does not purport to explain life's origins.-The statement you quote is over reaching I admit, however it is not a distortion, if, as you say, you accept the continuity. First life had to contain the preparations for evolution, thus the continuum. Evolution begins with first life, not just after life arrives, because first life contains the information permitting alterations, that allows for evolution. Of course, any theory of evolution does not explain the origin of life. There is a fine distinction here. We have quarreled about this before. You cannot disconnect origin from evolution.

Genome complexity: challenges naturalism

by dhw, Wednesday, September 23, 2015, 12:35 (3110 days ago) @ David Turell

dhw: QUOTE: “Aside from the obvious (and intriguing) challenge of understanding the enormous complexity of life's information payload, evolution purports to explain its origins.”-DAVID: The statement you quote is over reaching I admit, however it is not a distortion, if, as you say, you accept the continuity. First life had to contain the preparations for evolution, thus the continuum. Evolution begins with first life, not just after life arrives, because first life contains the information permitting alterations, that allows for evolution. Of course, any theory of evolution does not explain the origin of life. There is a fine distinction here. We have quarreled about this before. You cannot disconnect origin from evolution.-There is no quarrel between us about this. I have never disputed the continuity, but we both agree that the theory of evolution does not exclude God. Some atheists, however, try to hoodwink their readers by pretending that it does (hence the Dawkins quote). Your author is using the same device in order to discredit evolution. I object to any false statements which, whether intentionally or not, add unwarranted strength to an argument. The theory of evolution does NOT purport to explain life's origins, so why say that it does? The theory of natural selection does NOT explain the whole of life, so why say that it does? Recent discoveries will NOT bring an end to the acceptance of Darwin's theory of evolution (though they may well bring an end to the acceptance of his ideas on how evolution works), so why say that they will?

Genome complexity: challenges naturalism

by David Turell @, Wednesday, September 23, 2015, 14:49 (3110 days ago) @ dhw


> dhw: Your author is using the same device in order to discredit evolution. I object to any false statements which, whether intentionally or not, add unwarranted strength to an argument. The theory of evolution does NOT purport to explain life's origins, so why say that it does? The theory of natural selection does NOT explain the whole of life, so why say that it does? Recent discoveries will NOT bring an end to the acceptance of Darwin's theory of evolution (though they may well bring an end to the acceptance of his ideas on how evolution works), so why say that they will?-I know what the author was doing. But that still does not diminish the point (which is what I emphasize) that first life had to be setup to evolve. Evolutionary theory was not exclusive to Darwin the time of his book. It predated him. His theory provided for chance and by your own admission that is not likely. If his theory is emasculated why continue to give him sole credit for recognizing evolution as a probable process? Wallace's point of view is just as strong in my view.

Genome complexity: 'speed' code

by David Turell @, Wednesday, September 23, 2015, 20:06 (3110 days ago) @ David Turell

The speed with which a protein is made depends on which codon is used. Some cause more speed, some cause less speed of manufacture, and this speed controls folding to create function.-http://www.sciencedaily.com/releases/2015/09/150923134211.htm-"It was long known that almost every amino acid can be encoded by multiple synonymous codons and that every organism, from humans to fungi, has a preference for certain codons. The researchers found that more frequently used codons ? the "preferred codons" ? speed up the process of producing an amino acid chain, while less frequently produced codons slow the process. The use of either preferred or non-preferred codons is like having speed signs on the protein production highway: some segments need to be made fast and others slow.-"'The genetic code of nucleic acids is central to life, as it specifies the amino acid sequences of proteins," said Dr. Liu, the Louise W. Kahn Scholar in Biomedical Research. "By influencing the speed with which a protein is assembled from amino acid building blocks, the use of "fast" and "slow" codons can affect protein folding, which is the process that allows a protein to form the right shape to perform a specific function. This speed control mechanism makes sure that proteins are assembled and folded properly in different cells. Therefore, the genetic code not only specifies the sequence of amino acids but also the shape of the protein."-"The researchers found that proteins with identical amino acid sequences can have different functions if they are assembled at different speeds. This can have important implications for identifying human disease-causing mutations because this study indicates that a mutation does not have to change amino acid identity to cause a disease. In fact, most mutations in human DNA do not result in amino acid change.-"'Therefore, our study indicates that the new "code" -- the speed limit of assembly -- within the genetic code can dictate the ultimate function of a given protein," said Dr. Liu."-Comment: science is finding the genome more and more complex. With increasing complexity the likelihood of Darwinian chance evolution lessens to zero.

Genome complexity: challenges naturalism

by dhw, Thursday, September 24, 2015, 17:24 (3109 days ago) @ David Turell

dhw: Your author is using the same device in order to discredit evolution. I object to any false statements which, whether intentionally or not, add unwarranted strength to an argument. The theory of evolution does NOT purport to explain life's origins, so why say that it does? The theory of natural selection does NOT explain the whole of life, so why say that it does? Recent discoveries will NOT bring an end to the acceptance of Darwin's theory of evolution (though they may well bring an end to the acceptance of his ideas on how evolution works), so why say that they will?
-DAVID: I know what the author was doing. But that still does not diminish the point (which is what I emphasize) that first life had to be setup to evolve. Evolutionary theory was not exclusive to Darwin the time of his book. It predated him. His theory provided for chance and by your own admission that is not likely. If his theory is emasculated why continue to give him sole credit for recognizing evolution as a probable process? Wallace's point of view is just as strong in my view.-No problem with any of the above, so long as you agree that authors of all persuasions should refrain from making false statements in an attempt to boost their arguments.

Genome complexity: challenges naturalism

by David Turell @, Thursday, September 24, 2015, 17:58 (3109 days ago) @ dhw


> dhw: No problem with any of the above, so long as you agree that authors of all persuasions should refrain from making false statements in an attempt to boost their arguments.-Agreed. What has the problem between us is that I have been remiss in clearly pointing out which facts in an article I endorse by assuming you understand my point of view. Just because I present an article doesn't mean I agree with the author's conclusions. You have seen that in our battle over bacterial intelligence.

Genome complexity: challenges naturalism

by dhw, Friday, September 25, 2015, 16:26 (3108 days ago) @ David Turell

dhw: Your author is using the same device in order to discredit evolution. I object to any false statements which, whether intentionally or not, add unwarranted strength to an argument. The theory of evolution does NOT purport to explain life's origins, so why say that it does? The theory of natural selection does NOT explain the whole of life, so why say that it does? Recent discoveries will NOT bring an end to the acceptance of Darwin's theory of evolution (though they may well bring an end to the acceptance of his ideas on how evolution works), so why say that they will?

DAVID: I know what the author was doing. But that still does not diminish the point (which is what I emphasize) that first life had to be setup to evolve. Evolutionary theory was not exclusive to Darwin the time of his book. It predated him. His theory provided for chance and by your own admission that is not likely. If his theory is emasculated why continue to give him sole credit for recognizing evolution as a probable process? Wallace's point of view is just as strong in my view.-dhw: No problem with any of the above, so long as you agree that authors of all persuasions should refrain from making false statements in an attempt to boost their arguments.-DAVID: Agreed. What has the problem between us is that I have been remiss in clearly pointing out which facts in an article I endorse by assuming you understand my point of view. Just because I present an article doesn't mean I agree with the author's conclusions. You have seen that in our battle over bacterial intelligence.
-Thank you. I have also been remiss. I should have said right from the beginning that I do understand your point of view, and I do understand the argument the article is putting forward. I had assumed that you would assume that I had understood! I was simply too horrified by the gross error of fact to make it clear that I was changing the subject to falsification. All is now clear.

Genome complexity: challenges naturalism

by David Turell @, Friday, September 25, 2015, 18:25 (3108 days ago) @ dhw


> dhw: Thank you. I have also been remiss. I should have said right from the beginning that I do understand your point of view, and I do understand the argument the article is putting forward. I had assumed that you would assume that I had understood! I was simply too horrified by the gross error of fact to make it clear that I was changing the subject to falsification. All is now clear.-Still friendly opponents. Thank you.

Genome complexity: cell division

by David Turell @, Monday, October 05, 2015, 14:24 (3098 days ago) @ David Turell

A complex mechanical marvel. Not by chance:-http://www.sciencedaily.com/releases/2015/10/151002133158.htm-"In order to segregate chromosomes into the two emerging cells, the spindle itself needs a bipolar structure, and so the microtubules must be sorted to align with the long pole-to-pole axis of the spindle. This job is accomplished by kinesin-5, which can bind to two overlapping microtubules, linking them like a bar in the letter H, and directing them to the appropriate locations.-"For this study, the researchers took a detailed look at the physical forces generated by the motor protein as it helps organize the mitotic spindle.-"To do the sorting, kinesin-5 can link two anti-parallel microtubules, pushing them in opposite directions, so their minus ends move away from the spindle's center and toward the spindle's poles. The force exerted by kinesin-5 in that process hasn't been previously measured.-"By shining a laser light on a microscopic-sized plastic bead attached to a pair of microtubules linked by kinesin-5 molecules, the team tracked their activity and discovered that this force is a function of the microtubule overlap--the longer the overlap, the greater the force. "This is a way by which the cell can tune the amount of force it needs in order to build a nice balanced spindle structure," Forth says.-"Kinesin-5 can also link parallel microtubules, and the researchers found that in this case, it behaves differently. Rather than producing a pushing force, it generates a resisting force that can slow down the microtubules' motion. And here again, that force scales up with the length of overlap between the microtubules.-"'We believe that kinesin-5 has the ability to coordinate the speed of microtubules and keep them from going too fast or too slow," says Forth, likening the protein to a gear box in a car. "It helps coordinate and govern the speed and location of the microtubules in the spindle." As many kinesin-5 molecules work together directing microtubules, they become the governing force of the spindle formation."-Comment: In cell division the daughter cells must have exactly the same chromosomes, otherwise chaos. Error correction mechanisms are known to help if necessary.

Genome complexity: de novo or orphan genes

by David Turell @, Wednesday, February 17, 2016, 15:49 (2963 days ago) @ dhw

No one knows how they arise or how they work as part of the evolutionary process. this is because they are 'new', not related to any in he past:-http://www.evolutionnews.org/2016/02/reader_asks_are102596.html-"Despite these disagreements, de novo genes do exist. But when their origin -- where they came from -- is discussed, it reveals yet another assumption of evolutionary biologists. Evolutionists say, "Look, these orphan genes arose de novo. We can see how they might have been spliced together from similar DNA present elsewhere in the genome, or they might have come from non-coding DNA that has acquired a promoter or transcription factor binding site, and so is now expressed, and makes a functional protein, in the right place and at the right time." -"These sentences reveal the second assumption -- that the existence of these new genes indicates there are natural processes to make them. After all, it must be possible to splice or activate new sequences to make TRGs, because there are TRGs (taxonomically restricted genes) . -"That's an assumption of naturalism. The problem is there is no evidence to show that those proposed mechanisms actually work. There are no experiments that I know of to demonstrate that splicing yields functional products. Attempts in the lab show that splicing together even related protein domains yields non-functional products. Also, no one has shown that it is easy to acquire a promoter or transcription factor binding site so as to turn inactive, non-coding DNA into expressed, functional DNA. Getting a functional protein from random non-coding sequence is impossibly hard and would have to be demonstrated. If the function is regulating other genes via RNA, that would have to be proven to be feasible, too.-***-"Bear in mind that TRGs can be up to 10-20 percent of a taxonomic group's genome, and may encode many of the special proteins unique to that taxonomic group. That's a huge chunk of DNA to arise by natural processes alone, and a big challenge for common descent. I am thinking of the phylum Cnidaria here. All Cnidaria (sea anemones, jelly fish, and Hydra for example) have tentacles with specialized cells called cnidocytes or nematocysts, which eject a little barbed tubule with a toxin into whatever touches them. They use these cells to capture and immobilize their prey. Many of the specialized proteins needed to make the nematocysts are TRGs specific to the phylum Cnidaria. Cnidaria are among the oldest of all extant phyla. Was their origin unique?"-Comment: Origin still unknown. Lots to explain. Could they be designed as drivers of complexity?

Genome complexity: de novo or orphan genes

by David Turell @, Monday, April 09, 2018, 15:12 (2181 days ago) @ David Turell

Orphan genes are those which are not found in any other species,casting doubt on common descent:

http://darwins-god.blogspot.com/2018/04/brochosome-proteins-encoded-by-orphan.html

"In fact, there are many orphans, and while function can be difficult to identify, it has been found for many orphans. As science writer Helen Pilcher explained:

"In corals, jellyfish and polyps, orphan genes guide the development of explosive stinging cells, sophisticated structures that launch toxin-filled capsules to stun prey. In the freshwater polyp Hydra, orphans guide the development of feeding tentacles around the organism’s mouth. And the polar cod’s orphan antifreeze gene enables it to survive life in the icy Arctic.

"Up to a third of genomes have been found have been found to be unique, as this review explains:

Comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. Do such ‘orphan’ or ‘taxonomically-restricted’ genes comprise spurious, non-functional ORFs, or does their presence reflect important evolutionary processes? Recent studies in basal metazoans such as Nematostella, Acropora and Hydra have shed light on the function of these genes, and now indicate that they are involved in important species-specific adaptive processes.

"And this is yet another failed prediction of evolution, as this paper explains:

"The frequency of de novo creation of proteins has been debated. Early it was assumed that de novo creation should be extremely rare and that the vast majority of all protein coding genes were created in early history of life. However, the early genomics era lead to the insight that protein coding genes do appear to be lineage-specific. Today, with thousands of completely sequenced genomes, this impression remains.

***

"Since the Nelson-Velasco debate the orphan problem has just gotten worse. Consider, for example, brochosomes which are intricate, symmetric, secretory granules forming super-oily coatings on the integuments of leafhoppers. Brochosomes develop in glandular segments of the leafhopper’s Malpighian tubules.

"The main component of brochosomes, as shown in a recent paper, is proteins. And these constituent proteins, as well as brochosome-associated proteins, are mostly encoded by orphan genes.

"As the paper explains, most of these proteins “appear to be restricted to the superfamily Membracoidea, adding to the growing list of cases where taxonomically restricted genes, also called orphans, encode important taxon-specific traits.'”

Comment: If evolution was a totally natural process, it becomes very difficult to explain natural common descent if 10-20% of genes have no relatives in preceding generations of species. Direction by God fits.

Genome complexity: de novo or orphan genes

by dhw, Tuesday, April 10, 2018, 12:46 (2180 days ago) @ David Turell

QUOTES: "In corals, jellyfish and polyps, orphan genes guide the development of explosive stinging cells, sophisticated structures that launch toxin-filled capsules to stun prey. In the freshwater polyp Hydra, orphans guide the development of feeding tentacles around the organism’s mouth. And the polar cod’s orphan antifreeze gene enables it to survive life in the icy Arctic.”
"Up to a third of genomes have been found have been found to be unique, as this review explains:
Comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. Do such ‘orphan’ or ‘taxonomically-restricted’ genes comprise spurious, non-functional ORFs, or does their presence reflect important evolutionary processes? Recent studies in basal metazoans such as Nematostella, Acropora and Hydra have shed light on the function of these genes, and now indicate that they are involved in important species-specific adaptive processes.”

DAVID’s comment: If evolution was a totally natural process, it becomes very difficult to explain natural common descent if 10-20% of genes have no relatives in preceding generations of species. Direction by God fits.

Speciation involves innovation of some kind, and it seems to me perfectly reasonable to assume that innovations are triggered by the drive for survival and/or improvement, in accordance with the living conditions of the organisms involved. This is illustrated by all the examples. If common descent is true, then of course there will be departures from each new species’ ancestors, and these will in some way involve innovative changes to the structure and function of cells and genes. What is your proposal? The Arctic cod is still a cod, so did your God preprogramme cod anti-freeze 3.8 billion years ago? Or did he see a cod freezing and pop down to give it some brand new genes? But yes, you can say that fits (though one can’t help wondering why he found it necessary to provide the polar cod with anti-freeze when apparently all he wanted to do was produce the brain of Homo sapiens), but whatever he may have done to the cells could also have been done by his providing cells with the autonomous means to do exactly the same thing. As always, the complexity of such an autonomous mechanism offers a powerful argument for design, but I’d be surprised if you thought your God was incapable of doing it.

This post covers the arguments you have put forward on the ant thread, which we can now close.

Genome complexity: de novo or orphan genes

by David Turell @, Tuesday, April 10, 2018, 14:58 (2180 days ago) @ dhw

QUOTES: "In corals, jellyfish and polyps, orphan genes guide the development of explosive stinging cells, sophisticated structures that launch toxin-filled capsules to stun prey. In the freshwater polyp Hydra, orphans guide the development of feeding tentacles around the organism’s mouth. And the polar cod’s orphan antifreeze gene enables it to survive life in the icy Arctic.”
"Up to a third of genomes have been found have been found to be unique, as this review explains:
Comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. Do such ‘orphan’ or ‘taxonomically-restricted’ genes comprise spurious, non-functional ORFs, or does their presence reflect important evolutionary processes? Recent studies in basal metazoans such as Nematostella, Acropora and Hydra have shed light on the function of these genes, and now indicate that they are involved in important species-specific adaptive processes.”

DAVID’s comment: If evolution was a totally natural process, it becomes very difficult to explain natural common descent if 10-20% of genes have no relatives in preceding generations of species. Direction by God fits.

dhw: Speciation involves innovation of some kind, and it seems to me perfectly reasonable to assume that innovations are triggered by the drive for survival and/or improvement, in accordance with the living conditions of the organisms involved. This is illustrated by all the examples. If common descent is true, then of course there will be departures from each new species’ ancestors, and these will in some way involve innovative changes to the structure and function of cells and genes. What is your proposal? The Arctic cod is still a cod, so did your God preprogramme cod anti-freeze 3.8 billion years ago? Or did he see a cod freezing and pop down to give it some brand new genes? But yes, you can say that fits (though one can’t help wondering why he found it necessary to provide the polar cod with anti-freeze when apparently all he wanted to do was produce the brain of Homo sapiens), but whatever he may have done to the cells could also have been done by his providing cells with the autonomous means to do exactly the same thing. As always, the complexity of such an autonomous mechanism offers a powerful argument for design, but I’d be surprised if you thought your God was incapable of doing it.

This post covers the arguments you have put forward on the ant thread, which we can now close.

They are all forceful arguments for specific design. Whether God stepped in or gave the organisms inventive adaptive mechanisms, it doesn't matter. It is all at God's direction.

Genome complexity: de novo or orphan genes

by dhw, Wednesday, April 11, 2018, 12:29 (2179 days ago) @ David Turell

dhw: Speciation involves innovation of some kind, and it seems to me perfectly reasonable to assume that innovations are triggered by the drive for survival and/or improvement, in accordance with the living conditions of the organisms involved. This is illustrated by all the examples. If common descent is true, then of course there will be departures from each new species’ ancestors, and these will in some way involve innovative changes to the structure and function of cells and genes. What is your proposal? The Arctic cod is still a cod, so did your God preprogramme cod anti-freeze 3.8 billion years ago? Or did he see a cod freezing and pop down to give it some brand new genes? But yes, you can say that fits (though one can’t help wondering why he found it necessary to provide the polar cod with anti-freeze when apparently all he wanted to do was produce the brain of Homo sapiens), but whatever he may have done to the cells could also have been done by his providing cells with the autonomous means to do exactly the same thing. As always, the complexity of such an autonomous mechanism offers a powerful argument for design, but I’d be surprised if you thought your God was incapable of doing it.

DAVID: They are all forceful arguments for specific design. Whether God stepped in or gave the organisms inventive adaptive mechanisms, it doesn't matter. It is all at God's direction.

It matters to anyone who thinks it matters. As indeed does the question of whether God exists or not. Hence this website.

Genome complexity: de novo or orphan genes

by David Turell @, Wednesday, April 11, 2018, 20:40 (2179 days ago) @ dhw

dhw: Speciation involves innovation of some kind, and it seems to me perfectly reasonable to assume that innovations are triggered by the drive for survival and/or improvement, in accordance with the living conditions of the organisms involved. This is illustrated by all the examples. If common descent is true, then of course there will be departures from each new species’ ancestors, and these will in some way involve innovative changes to the structure and function of cells and genes. What is your proposal? The Arctic cod is still a cod, so did your God preprogramme cod anti-freeze 3.8 billion years ago? Or did he see a cod freezing and pop down to give it some brand new genes? But yes, you can say that fits (though one can’t help wondering why he found it necessary to provide the polar cod with anti-freeze when apparently all he wanted to do was produce the brain of Homo sapiens), but whatever he may have done to the cells could also have been done by his providing cells with the autonomous means to do exactly the same thing. As always, the complexity of such an autonomous mechanism offers a powerful argument for design, but I’d be surprised if you thought your God was incapable of doing it.

DAVID: They are all forceful arguments for specific design. Whether God stepped in or gave the organisms inventive adaptive mechanisms, it doesn't matter. It is all at God's direction.

dhw: It matters to anyone who thinks it matters. As indeed does the question of whether God exists or not. Hence this website.

Ten years of this website.

Genome complexity: de novo or orphan genes

by David Turell @, Saturday, February 23, 2019, 19:57 (1861 days ago) @ David Turell

More comment:

https://www.cambridge.org/core/books/next-generation-systematics/next-generation-apomor...

"Shortly after the publication of the first whole genome in 1995, it became clear that species possessed many more taxonomically unique, or restricted, gene sequences than expected. When seven whole genomes had been published, R. F. Doolittle, a molecular biologist of many decades’ experience, commented: ‘I am surprised that so many open reading frames remain as unidentified [i.e. unique] reading frames’. Five years later, when 60 whole genomes had been sequenced, he called taxonomically unique sequences ‘the biggest surprise in genome sequencing’.

" Today, with whole-genome sequencing further facilitated by next generation technologies, these taxonomically restricted genes, also known as orphan genes, or ‘ORFans’) continue to be discovered in every newly sequenced species genome. These genes represent one of the most intriguing aspects of systematics, lying at the intersection of genomics, genetics, comparative and structural biology, phylogenetics and evolution. Yet, by their very nature, they are difficult to study using conventional comparative approaches and attract little research funding.

My comment: They are part of 'so-called junk' DNA and definitely appear to have functionality. As orphans they do not come from preceding organisms in evolution. This is not what Darwin expected:

"'a chapter on orphan and taxonomically restricted genes in Next Generation Systematics (Cambridge University Press 2016) by Richard Buggs and Paul Nelson. There they ventured a prediction: “We suspect that if one’s model system or species of study does something unique and interesting, TRGs [taxonomically restricted genes, aka orphans] will be at least partially responsible, and worth seeking out.'”

https://uncommondescent.com/evolution/id-predictions-on-orphan-genes-and-symbiosis/

"…the ANG [accessory nidimental gland] of E. scolopes is highly derived and shows an elevated evolutionary accumulation in both its coding (novel gene formation) and noncoding (turnover of the regulatory sequence) complements. The ANG is a secretory organ within the female reproductive system containing a bacterial consortium that is deposited into the egg capsule and is believed to play a role in defense from fouling and/or pathogens during embryogenesis (7, 8, 15, 16). Taxonomically restricted (i.e., orphan) genes have contributed to the evolution of unique tissues and organs in a number of animals."

Genome complexity: de novo or orphan genes

by David Turell @, Thursday, January 21, 2021, 23:07 (1163 days ago) @ David Turell

More from Richard Buggs: (David Turell, 2019-02-23, 19:57)

https://inference-review.com/article/the-origin-of-novel-genes

"The four studies find that organisms with different morphologies possess different sets of genes. Given that genes provide much of the information encoding the morphology of living organisms, this finding may not seem a surprise. That novel genes do not accumulate with Darwinian gradualism in the phylogeny is perhaps more surprising. The authors describe bursts of innovation: upon the origin of placental mammals, 357 novel genes; upon the origin of the metazoan, 1,189 novel genes; upon the origin of the land plants, 1,167 novel genes; and upon the origin of the flowering plants, 2,525 novel genes.

"Equally surprising is evidence that the patterns of presence and absence of many genes in these studies do not form a nested hierarchy congruent with the accepted phylogeny. Particular genes often appear in more than one clade (Figure 1). This leads the authors to infer massive gene losses and frequent horizontal gene transfer in the history of life.

"The unexpected nature of these findings was not lost on the authors of the studies, nor the editors of the journals that published their manuscripts. Three of the paper titles emphasize unexpected novelty and one emphasizes unexpected loss. But all four show similar patterns. More is revealed in each than a single title can convey.

***

"In the 1850s, Charles Darwin considered it obvious that the morphological variation of life was continuous: “all the parts and organs of many independent beings” are “linked together by graduated steps.”

***

"It is far from clear how these homology groups might be linked in graduated steps. The evolution of novel genes is a subject with a substantial literature all its own, which has recently shifted from the view that all new genes begin as duplicates of pre-existing genes to a view that many genes evolve de novo from noncoding sequences. The mechanisms underlying this process are not well understood.

***

"Rather than emerging gradually, a few at a time, the evidence presented in these four papers suggests the occurrence of punctuated bursts. At every major phylogenetic node that was examined, the appearance of hundreds, and in some cases thousands, of novel homology groups was detected.

"Evolution by bursts is, of course, not expected if natural selection is the main driver. “[N]atural selection acts only by taking advantage of slight successive variations,” Darwin remarked; “she can never take a great and sudden leap, but must advance by the short and sure, though slow steps.”5 The findings presented in these papers suggest otherwise. It seems that the evolution of life is characterized by leaps involving large numbers of novel homology groups.

***

"The fossil record depicts the appearance of the first angiosperms as a sudden event, with no clear progenitors. This was known, in part, to Darwin, who famously complained to the director of Kew Gardens in 1879 that the origin of the dicotyledonous angiosperms was an “abominable mystery.”7 The mystery has since deepened to include all other angiosperms.

***

"These studies by the teams of Holland and Paps are not alone in finding bursts of novel genes in the history of life. In a paper published earlier this year, Zhang et al. conducted an analysis of plants similar to Bowles et al., with better sampling of charophytes and bryophytes.10 Despite using different gene clustering methods and a smaller set of species, they found gene gains at key nodes on similar orders of magnitude.

***

"ALL FOUR STUDIES under review found massive gene losses for phylogenetic nodes at the base of the major groups of living organisms. This suggests that major evolutionary transitions do not occur solely by means of tinkering with existing genes. Instead, it seems that vast numbers of existing genes are jettisoned and replaced by entirely different ones. Such processes would represent a radical overhaul in the genetic composition of organisms. How this might be accomplished is another mystery.

***

"Bowles et al. found that 323 homology groups were present in fungal and land plant genomes, but absent from all other taxa.12 Instead of being lost in the lineages between fungi and land plants, the genes could simply have jumped. This may turn out to be a more elegant solution to the problem.

"The incongruence between patterns in the absence or presence of homology groups and widely accepted phylogenies raises a broader issue. A single phylogeny is clearly an inadequate model for the history of life, but there is no obvious replacement. This question is wide open."

Comment: Gould's gaps and punctuation stares at you in your face. Behe laughs about the losses. This question is not 'wide open' as this discontinuity is perfect evidence of God the designer at work stepping in.

Genome complexity: bacterial controls in horizontal transfe

by David Turell @, Thursday, March 09, 2023, 00:32 (387 days ago) @ David Turell

And also controls over enemy DNA:

https://phys.org/news/2023-03-insights-bacterial-immune.html

"Bacteria, for example, take up foreign DNA through a process called horizontal gene transfer, which is much faster than the vertical inheritance from generation to generation.

"However, every living organism also faces risks by taking up foreign genetic information, as it could potentially be dangerous if, for example, important genes are damaged by integration into its own chromosome, resulting in major disadvantages for the organism as a whole. Therefore, bacteria have developed numerous mechanisms protecting them from absorbing harmful DNA. Many of the molecular processes involved were discovered in recent years, leading to the recent coinage of the term "bacterial immune system."

***


"Using the bacterium Corynebacterium glutamicum as an example, the researchers showed that the so-called Mks protein system has an additional element that can bind to plasmid DNA and cut it apart.

***

"Plasmids are small, usually ring-shaped, double-stranded DNA molecules that can replicate independently of the chromosome in their host cell. They play an important role in the ecology and evolution of bacteria, as they are an important vehicle of lateral gene transfer, enabling the rapid transfer of genetic information and thus the expression of selection advantages. In principle, all bacteria can exchange plasmids with each other even across species.

"This happens directly from bacterium to bacterium via a transfer mechanism known as conjugation. Both advantageous and disadvantageous plasmids utilize such bridges between bacterial cells to switch from one bacterium to another.

***

"'In previous research, we have investigated systems that are generally involved in the organization of DNA in bacterial cells and, among other things, ensure the packaging of genetic information into the compressed form of chromosomes," Weiß continues.

"In this context, the research team obtained initial indications that C. glutamicum possesses two such systems, one of which is not involved in the organization of the chromosome, but can prevent the multiplication of certain plasmids, although the mechanism responsible for this was previously unknown.

"Now, the Kiel researchers, together with experts led by Dr. Anne Marie Wehenkel from the Institut Pasteur in Paris, have discovered the DNA scissors of the Mks system in a structural study. "We were able to prove experimentally that this new subunit of the Mks system forms a specific protein, a so-called nuclease, which can cut DNA. This element has the task of degrading plasmids in order to keep harmful DNA away from the bacterial cell, while the other components of the Mks system are important for the recognition of plasmid DNA," Weiß says.

***

"'Bacteria use certain plasmids as a source of new, not immediately vital, genetic information. It is therefore obvious that a defense mechanism must be selective and not destroy all plasmids," says Bramkamp.

"'We were able to prove that in C. glutamicum there is indeed a directed selection according to beneficial and detrimental genetic information. When we artificially switched off the Mks system and thus all plasmids remained in the bacterial cells, detrimental effects on the cell, possibly triggered by DNA stress, were evident. However, these did not occur when the defense mechanism was active," Bramkamp continues.

'With the current work, the Kiel researchers are presenting important new findings about the bacterial immune system overall, which expand the understanding of plasmids as mediators of not only beneficial but also harmful genetic information. In future, they want to investigate which molecular mechanisms allow bacterial cells to differentiate between "good" and "bad" mobile DNA."

Comment: an advance in Shapiro's work on how bacteria handle additions to their DNA.

Genome complexity: bacteria make elecricity from air

by David Turell @, Thursday, March 09, 2023, 16:10 (386 days ago) @ David Turell

Using available hydrogen:

https://www.sciencealert.com/soil-bacteria-discovery-could-allow-us-to-produce-electric...


"It may sound surprising, but when times are tough and there is no other food available, some soil bacteria can consume traces of hydrogen in the air as an energy source.

"In fact, bacteria remove a staggering 70 million tonnes of hydrogen yearly from the atmosphere, a process that literally shapes the composition of the air we breathe.

"'We have isolated an enzyme that enables some bacteria to consume hydrogen and extract energy from it, and found it can produce an electric current directly when exposed to even minute amounts of hydrogen.

***

"Prompted by this discovery, we analyzed the genetic code of a soil bacterium called Mycobacterium smegmatis, which consumes hydrogen from air.

"Written into these genes is the blueprint for producing the molecular machine responsible for consuming hydrogen and converting it into energy for the bacterium. This machine is an enzyme called a "hydrogenase", and we named it Huc for short.

"Hydrogen is the simplest molecule, made of two positively charged protons held together by a bond formed by two negatively charged electrons. Huc breaks this bond, the protons part ways, and the electrons are released.

"In the bacteria, these free electrons then flow into a complex circuit called the "electron transport chain", and are harnessed to provide the cell with energy.

***

"Hydrogen represents only 0.00005 percent of the atmosphere. Consuming this gas at these low concentrations is a formidable challenge, which no known catalyst can achieve. Furthermore, oxygen, which is abundant in the atmosphere, poisons the activity of most hydrogen-consuming catalysts.

***

"With Huc isolated, we set about studying it in earnest, to discover what exactly the enzyme is capable of. How can it turn the hydrogen in the air into a sustainable source of electricity?

"Remarkably, we found that even when isolated from the bacteria, Huc can consume hydrogen at concentrations far lower even than the tiny traces in the air. In fact, Huc still consumed whiffs of hydrogen too faint to be detected by our gas chromatograph, a highly sensitive instrument we use to measure gas concentrations.

"We also found Huc is entirely uninhibited by oxygen, a property not seen in other hydrogen-consuming catalysts.

***

"""In short, this research shows how a fundamental discovery about how bacteria in soils feed themselves can lead to a reimagining of the chemistry of life."

Comment: this is how extremophiles can survive using enzymes of this sort.

Genome complexity: corals filter new mutations

by David Turell @, Friday, March 10, 2023, 19:54 (385 days ago) @ David Turell

Keep the good, filter out the bad:

https://phys.org/news/2023-03-youre-stuck-genome-corals.html

"Some corals live to be hundreds, and even thousands, of years old. They were born with genes that were successful back in their parent's generation, so how can these old corals still be successful now? Especially in a changing climate? It's possible that the generation and the filtering of mutations that occur in different parts of a big coral act as a proving ground for adaptive genetics for the future.

***

"Nearly every animal must make a living with a set of genes that remains virtually unchanged during their lifetime, but a recent study of tropical reef building corals shows something different. These very long-lived animals are constantly changing and testing their genes—and some of these changes make it into the next generation. In this way a centuries-old coral might be a cauldron of genetic innovation, and it might help prepare them for climate change.

***

"The López-Nandam study found that the mutations that made it into the next coral generation had far fewer protein changes. This means that the corals were somehow filtering out the most likely deleterious mutations, and passing on changes that did not hurt the coral cells or that potentially benefited them.


"Overall, this study agrees with previous studies that found mutations in the tissues of large, long-lived corals are evolutionarily important. These mutations can add to the genetic diversity of coral populations and increase their ability to adapt to new conditions. In most animals this process also happens when offspring inherit new mutations that happen in the eggs and sperm of their parents, but takes many generations.

"The López-Nandam study goes a step further and shows that this adaptive process can happen within a single coral colony in a single generation—mutations are filtered to remove the harmful ones, potentially giving rise to patches of coral with new adaptive alleles…maybe even new mutations that can help counteract some of the stresses of climate-induced heat waves."

Comment: a different form of editing than in bacteria. Actively screening new mutations that serendipitously pop up.

Genome complexity: stop is not always stop

by David Turell @, Friday, May 23, 2014, 15:54 (3598 days ago) @ David Turell

There are three recognized stop codons. But in some organisms they mean keep on coding.-http://www.sciencedaily.com/releases/2014/05/140522141422.htm-This means the standard model of DNA is not exact all through living organisms.-"All along, we presumed that the code or vocabulary used by organisms was universal, applying to all branches of the tree of life, with vanishingly few exceptions," said DOE JGI Director Eddy Rubin, and senior author on the Science paper. "We have now confirmed that this just isn't so. There is a significant portion of life that uses different vocabularies where the same word means different things in different organisms."

Genome complexity in embryology

by David Turell @, Thursday, April 16, 2015, 01:28 (3271 days ago) @ David Turell

A video showing the process of cell division of C. elegans, a tiny Nematode worm of about 1,000 cells, including nerves. It really raises the issue of how multicellularity developed, allowing all the different types of specialized cells required, all coming from one fertilized egg.-https://www.youtube.com/watch?v=QDQ0NJQ_z3U&feature=youtu.be

Genome complexity in embryology

by David Turell @, Thursday, April 23, 2015, 01:45 (3264 days ago) @ David Turell

Development of form in the embryo is not dictated by the genes, according to Michael Denton!:-"In addition, it is well established that the embryo is shaped by epigenetic biophysical and biomechanical forces and NOT by the genes. Yes, the genes provide the raw material -- base matter -- but it is the shaping of this raw matter by physical forces that gives us the specific architecture of the embryo. These forces arise from the emergent viscoelastic properties of individual embryonic cells and cell collectives -- layers of cells, clumps of cells, etc. Self-evidently the physical properties of one cell (the initial egg) are very different from the physical properties of a ball of cells (the morula), and a hollow ball (blastula) has different properties again.-"This succession of unique physical properties in the developing embryo that occurs during ontogeny is not specified in the genome. What is also very intriguing about the biophysical and biomechanical forces that shape embryos is that they represent a clear case of top-down causation where the overall biomechanical state of the embryo influences downwardly the behavior and state of all the constituents in the embryo. Even the expression of genes is now known to be regulated to a degree by the mechanical state of the whole embryo itself and its constituent cells. Hence my interest in Aristotle's substantial agencies, which shape "base matter" into the higher architecture of life." (my bold)-http://www.evolutionnews.org/2015/04/aristotle_redis095391.html

Genome complexity in embryology

by dhw, Thursday, April 23, 2015, 12:44 (3263 days ago) @ David Turell

DAVID: [UOTE] Even the expression of genes is now known to be regulated to a degree by the mechanical state of the whole embryo itself and its constituent cells." (my bold)-As I keep emphasizing, the concept of the inventive mechanism entails INVENTION. Once an invention functions, the behaviour of the cells will presumably repeat itself, i.e. will be or will at least appear to be automatic, though we have no idea to what extent they are mindful. An analogy might be factory workers simply doing their jobs. The idea of the IM arises from the fact that, as repeated ad nauseam, many scientists believe cells to have their own form of intelligence, and since no-one has ever observed innovation, I am suggesting that under certain conditions, this intelligence may have produced innovation. I am not suggesting that every single biological process has to be reinvented in every single individual by every single cell community!

Genome complexity in embryology

by David Turell @, Thursday, April 23, 2015, 18:58 (3263 days ago) @ dhw

DAVID: [UOTE] Even the expression of genes is now known to be regulated to a degree by the mechanical state of the whole embryo itself and its constituent cells." (my bold)
> 
> dhw:... I am suggesting that under certain conditions, this intelligence may have produced innovation. I am not suggesting that every single biological process has to be reinvented in every single individual by every single cell community!-I know you are not suggesting that. My point is that a whole area of knowledge is developing to suggest that physics principals dictate form in the development of the embryo. It is in line with Sheldrake's proposal of 'morphic resonance', something which helps the embryo take a certain form, and none other. This is one of the mysteries of embryology. Cells change DNA under instruction and becomes organs. What overall guidance joins them together as an individual? Hox genes control limb structure as an example, but total body form? Unknown. Another reason why I have turned to a planning mind as a source.

Genome complexity in embryology

by David Turell @, Friday, April 24, 2015, 18:05 (3262 days ago) @ David Turell

A new discovery is that the organelle, the centriole, which organizes mitosis, comes from sperm in the zygote, and seems to drive embryogenesis for up to 10 generations of cells and therefore is suspected of carrying information for the whole process of development. This is outside the genome:-http://www.sciencedaily.com/releases/2015/04/150424085630.htm-"Perhaps best known for their role in cell division, centrioles ensure that chromosomes are properly passed on to the new daughter cells. However, they are also found in cilia, the long eyelash-like structures that allow many cells in the body to signal to their neighbors and other cells to exhibit motility, e.g. in cells that line the respiratory tracts. During reproduction, both parents equally contribute genetic material, while the female egg donates most of the cell organelles, such as mitochondria. However, the centrioles of the newly fertilized embryo come exclusively from the male's sperm, bringing with them any malfunctions to the first embryo cells.-"The lab of Pierre Gönczy at EPFL's Swiss Institute for Experimental Cancer Research has found that centrioles can carry such information beyond the first cells to many of a developing embryo to several cell generations. The study focused on the worm C. elegans, which is commonly used as a model organism for embryonic development and human genetic diseases. As in other species, including humans, centrioles in C. elegans are only contributed by sperm cells. Gönczy's team wanted to know how far do these "original" centrioles last across the cell divisions that turn a fertilized egg into a fully formed embryo.-"Gönczy's team imaged the fluorescent signals at different cell divisions of the developing embryos, and discovered that paternally contributed centriole proteins can actually persist up to ten cell generations. The data show for the first time that centrioles are remarkably persistent in the developing embryo.-"Even more intriguing are the implications the study has for biology at large, as it raises the possibility that centrioles, persisting across several cell cycles, could effectively be a non-genetic information carrier. If this were confirmed, it could represent a paradigm shift in the way we think and understand the biology of an organelle that has been present across eukaryotic evolution."-Complexer and complexer

Genome complexity in embryology

by dhw, Friday, April 24, 2015, 22:14 (3262 days ago) @ David Turell

DAVID:

Even the expression of genes is now known to be regulated to a degree by the mechanical state of the whole embryo itself and its constituent cells." (my bold)-dhw:... I am suggesting that under certain conditions, this intelligence may have produced innovation. I am not suggesting that every single biological process has to be reinvented in every single individual by every single cell community!-DAVID: I know you are not suggesting that. My point is that a whole area of knowledge is developing to suggest that physics principals dictate form in the development of the embryo. It is in line with Sheldrake's proposal of 'morphic resonance', something which helps the embryo take a certain form, and none other. This is one of the mysteries of embryology. Cells change DNA under instruction and becomes organs. What overall guidance joins them together as an individual? Hox genes control limb structure as an example, but total body form? Unknown. Another reason why I have turned to a planning mind as a source.-MY RESPONSE, WHICH FOR SOME REASON INSISTS ON BEING ITALICIZED:If I may say so, an excellent summary of the problem. Once an organ/organism functions, the cells repeat the form and all the procedures. This is observable. How did the organ/organism come into being in the first place? Unknown. But cells HAVE to cooperate if the innovation is to work. Sheer luck (random mutations)? That takes some believing. Preprogrammed 3.7 billion years ago? That takes some believing. God fiddling around with each individual organism? That takes some believing. Intelligent cells working it out among themselves? Mhmmmm....

Genome complexity in embryology

by David Turell @, Saturday, April 25, 2015, 01:00 (3262 days ago) @ dhw

David Cells change DNA under instruction and becomes organs. What overall guidance joins them together as an individual? Hox genes control limb structure as an example, but total body form? Unknown. Another reason why I have turned to a planning mind as a source.[/i]
> 
> dhw:MY RESPONSE, WHICH FOR SOME REASON INSISTS ON BEING ITALICIZED:If I may say so, an excellent summary of the problem. Once an organ/organism functions, the cells repeat the form and all the procedures. This is observable. ... Intelligent cells working it out among themselves? Mhmmmm....-Take out the '>' and it won't be italicized. My question to your question: how did cells become intelligent? Or were they given intelligent information to work with? I know you will agree the intelligence did not appear by chance.

Genome complexity in embryology

by dhw, Sunday, April 26, 2015, 13:08 (3260 days ago) @ David Turell

dhw: Once an organ functions, the cells repeat the form and all the procedures. This is observable. How did the organ come into being in the first place? Unknown. But cells HAVE to cooperate if the innovation is to work. Sheer luck (random mutations)? That takes some believing. Preprogrammed 3.7 billion years ago? That takes some believing. God fiddling around with each individual organism? That takes some believing. Intelligent cells working it out among themselves? Hmmmm.... -DAVID: My question to your question: how did cells become intelligent? Or were they given intelligent information to work with? I know you will agree the intelligence did not appear by chance.-As usual, you ignore the problem of how evolution may have progressed and scurry to the safe ground of origins. But I will give you the same answer as I have always given you: I don't know how cells became intelligent. How did first cause energy “become intelligent”? You will say it just is. You might as well say cells just are. It's not an answer. Neither of us has an answer. Now back to evolution. A 3.7-billion-year computer programme for every single innovation including the weaverbird's nest? God dabbling with the weaverbird etc.? God preprogramming or separately creating the whale in order to produce humans? Do you really find such hypotheses convincing?

Genome complexity in embryology

by David Turell @, Sunday, April 26, 2015, 21:14 (3260 days ago) @ dhw

DAVID: My question to your question: how did cells become intelligent? Or were they given intelligent information to work with? I know you will agree the intelligence did not appear by chance.
> 
> dhw: As usual, you ignore the problem of how evolution may have progressed and scurry to the safe ground of origins. But I will give you the same answer as I have always given you: I don't know how cells became intelligent.-But they obviously operate using intelligent information. I find it beyond belief it developed de novo by chance. You don't accept chance either. ->dhw: How did first cause energy “become intelligent”? You will say it just is. You might as well say cells just are. It's not an answer. Neither of us has an answer.-I have accepted a logical answer for me. You just throw your hands up and give up. To me it is can incontrovertible fact that operating with intelligent information, requires supplied information. I don't see why you can't accept that and take the next step.-> dhw: Now back to evolution. A 3.7-billion-year computer programme for every single innovation including the weaverbird's nest? God dabbling with the weaverbird etc.? God preprogramming or separately creating the whale in order to produce humans? Do you really find such hypotheses convincing?-Again confusing the issue. I've admitted to accepting some type of evolutionary process to reach today's reality. I've admitted I don't know how it works, or why whales were produced. Living organisms are obviously wildly inventive, either by directed development or by innovation semi-independently developed. I only know that it requires conscious planning.

Genome complexity in embryology

by dhw, Monday, April 27, 2015, 21:36 (3259 days ago) @ David Turell

dhw: How did first cause energy “become intelligent”? You will say it just is. You might as well say cells just are. It's not an answer. Neither of us has an answer.
DAVID: I have accepted a logical answer for me. You just throw your hands up and give up. To me it is can incontrovertible fact that operating with intelligent information, requires supplied information. I don't see why you can't accept that and take the next step.-If I had given up, this website would not exist. There is no more logic to the answer that God's intelligence is “first cause” than there is to the answer that cellular intelligence evolved. We have discussed your use of “information” before: one is the information that comes from within, which I would call intelligence, and the other is the information that comes from outside, which is what intelligence processes. The next step is: where did the inside intelligence come from? Round we go. (See also “Evolution v Creationism”)-dhw: Now back to evolution. A 3.7-billion-year computer programme for every single innovation including the weaverbird's nest? God dabbling with the weaverbird etc.? God preprogramming or separately creating the whale in order to produce humans? Do you really find such hypotheses convincing?-DAVID: Again confusing the issue. I've admitted to accepting some type of evolutionary process to reach today's reality. I've admitted I don't know how it works, or why whales were produced. Living organisms are obviously wildly inventive, either by directed development or by innovation semi-independently developed. I only know that it requires conscious planning.-Either wildly inventive organisms are wildly inventive or they are automatons obeying your God's instructions. I don't see how a weaverbird can be responsible for half a nest. I agree about conscious planning, but find it unlikely that God planned the weaverbird's nest 3.7 billion years ago, even before the weaverbird existed. I appreciate all your admissions, but wish you would stop using euphemisms such as “guided” and “directed” to gloss over the fact that this entails preprogramming or direct dabbling. We English cowboys shoot from the hip - none of your fancy twiddles and twirls.

Genome complexity in embryology

by David Turell @, Tuesday, April 28, 2015, 02:14 (3259 days ago) @ dhw


> dhw: If I had given up, this website would not exist. There is no more logic to the answer that God's intelligence is “first cause” than there is to the answer that cellular intelligence evolved. We have discussed your use of “information” before: one is the information that comes from within, which I would call intelligence, and the other is the information that comes from outside, which is what intelligence processes. The next step is: where did the inside intelligence come from? -Exactly! As life originated (we don't have any direct evidence of 'how'), did it develop its 'intelligence' by hunt-and-peck? By chance? How did the earliest collection of cooperative proteins learn by experience, if it did? Within the collection of these proteins was there any ability to evaluate sensory input, if there was any sensory input. See the 'chicken and egg' problem expressed in my last post of 15 minutes ago.-> 
> dhw: Either wildly inventive organisms are wildly inventive or they are automatons obeying your God's instructions.....but wish you would stop using euphemisms such as “guided” and “directed” to gloss over the fact that this entails preprogramming or direct dabbling. We English cowboys shoot from the hip - none of your fancy twiddles and twirls.-I've admitted to preprogramming or dabbling all along. Guided and directed fit the bill.

Genome complexity in embryology

by dhw, Wednesday, April 29, 2015, 13:13 (3257 days ago) @ David Turell

DAVID: As life originated (we don't have any direct evidence of 'how'), did it develop its 'intelligence' by hunt-and-peck? By chance? How did the earliest collection of cooperative proteins learn by experience, if it did? Within the collection of these proteins was there any ability to evaluate sensory input, if there was any sensory input. See the 'chicken and egg' problem expressed in my last post of 15 minutes ago.-No problem asking the questions. No way of answering them. How did energy come by its intelligence? How did it know about proteins and DNA and RNA and brains and livers and penises and weaverbirds' nests, with some of these planned in advance billions of years before cell communities switched on their computers? At least one can imagine how organisms might learn by experience and improve through innovations, as evolution demonstrates. A God following the same learning curve would seem more convincing to me than your UI who preprogrammes humans from the start, but also preprogrammes plovers and platypuses, whales and weaverbirds for reasons you cannot discern. -dhw: Either wildly inventive organisms are wildly inventive or they are automatons obeying your God's instructions.....but wish you would stop using euphemisms such as “guided” and “directed” to gloss over the fact that this entails preprogramming or direct dabbling. We English cowboys shoot from the hip - none of your fancy twiddles and twirls.-DAVID: I've admitted to preprogramming or dabbling all along. Guided and directed fit the bill.-You have,but you stopped using those terms when I started pushing the unlikelihood of a 3.7-billion-year computer programme, and the problem of drawing the line between dabbling and separate creation. “Guided” and “directed” are so gently vague that they mask the colossal implications and the problems attached to them.

Genome complexity in embryology

by David Turell @, Wednesday, April 29, 2015, 18:32 (3257 days ago) @ dhw

dhw: A God following the same learning curve would seem more convincing to me than your UI who preprogrammes humans from the start, but also preprogrammes plovers and platypuses, whales and weaverbirds for reasons you cannot discern.-How do you know God has a learning curve? No theologian would claim that, why should you? 
> 
> dhw: Either wildly inventive organisms are wildly inventive or they are automatons obeying your God's instructions.....but wish you would stop using euphemisms such as “guided” and “directed” to gloss over the fact that this entails preprogramming or direct dabbling. We English cowboys shoot from the hip - none of your fancy twiddles and twirls.
> 
> DAVID: I've admitted to preprogramming or dabbling all along. Guided and directed fit the bill.
> 
> dhw; You have,but you stopped using those terms when I started pushing the unlikelihood of a 3.7-billion-year computer programme, and the problem of drawing the line between dabbling and separate creation. “Guided” and “directed” are so gently vague that they mask the colossal implications and the problems attached to them.-They are your problems, not mine. I don't know why you try so hard to decipher God's exact role in evolution. I don't think anyone knows except Him. It seems He used an evolutionary process. Dayenu!

Genome complexity in embryology

by dhw, Thursday, April 30, 2015, 20:59 (3256 days ago) @ David Turell

dhw: A God following the same learning curve would seem more convincing to me than your UI who preprogrammes humans from the start, but also preprogrammes plovers and platypuses, whales and weaverbirds for reasons you cannot discern.
DAVID: How do you know God has a learning curve? No theologian would claim that, why should you?-If a hypothesis seems to me “more convincing”, that does not mean it has become knowledge! I don't even know if God exists. I can't believe I'm the first person ever to conceive of a God who learns as he goes along, and some forms of process theology do suggest that. But frankly, I'm surprised that someone who claims to think for himself should be so dependent on what theologians claim. -DAVID: I've admitted to preprogramming or dabbling all along. Guided and directed fit the bill.
dhw; You have,but you stopped using those terms when I started pushing the unlikelihood of a 3.7-billion-year computer programme, and the problem of drawing the line between dabbling and separate creation. “Guided” and “directed” are so gently vague that they mask the colossal implications and the problems attached to them.
DAVID: They are your problems, not mine. I don't know why you try so hard to decipher God's exact role in evolution. I don't think anyone knows except Him. It seems He used an evolutionary process. Dayenu!-I try so hard because you have categorically stated God's exact role in evolution, and I am not convinced. You tell us that all the complexities are the result of God preprogramming the first living cells with every possible innovation over the last 3.7 billion years, or alternatively that these innovations are the result of his personal intervention, all for the purpose of producing humans. You even reject the alternative proposal that he might have endowed cells with an autonomous inventive mechanism, and you try to water it down to semi-autonomous in order to ensure that God is always in control. But when your theory is shown to be riddled with problems, you tell me not to bother!

Genome complexity in embryology

by David Turell @, Friday, May 01, 2015, 02:38 (3256 days ago) @ dhw

DAVID: How do you know God has a learning curve? No theologian would claim that, why should you?
> 
> dhw: If a hypothesis seems to me “more convincing”, that does not mean it has become knowledge! I don't even know if God exists....But frankly, I'm surprised that someone who claims to think for himself should be so dependent on what theologians claim.-Whitehead's process theology might claim God learns by experience. I'm not claiming to be dependent on theologians in the comment I gave. Other than the possibility of Whitehead, whom I have not studied, I've not heard that God has a learning curve and I don't know if He does or not. Why did you twist my comment?-> DAVID: They are your problems, not mine. I don't know why you try so hard to decipher God's exact role in evolution. I don't think anyone knows except Him. It seems He used an evolutionary process. Dayenu!
> 
> dhw: I try so hard because you have categorically stated God's exact role in evolution, and I am not convinced. ... But when your theory is shown to be riddled with problems, you tell me not to bother!-The problem is I liked my theory, and don't accept your problems with it. I've said I accept the probability of an evolutionary process because the appearance of organisms from simple to complex over time is strongly suggestive of evolution. That doesn't mean I understand how a guided evolutionary process works, but that is what I think it is.

Genome complexity in embryology: neural crest cells

by David Turell @, Wednesday, May 06, 2015, 03:19 (3250 days ago) @ David Turell

More and more complexity. Pluripotential neural crest cells:-http://www.sciencedaily.com/releases/2015/04/150430145125.htm-"'Neural crest cells never had their potential restricted at all," LaBonne said. "We believe a small population of early stem cells were set aside, so that when the time came, their immense developmental potential could be unleashed to create new features characteristic of vertebrates."-"Acquisition of neural crest cells more than 500 million years ago led vertebrates to evolve and leave behind less complex life forms (simple aquatic filter feeders, much like today's sea squirts and lancelets). With these cells, animals developed important new features such as a skull to house a complex brain, jaws for predation, a complex peripheral nervous system and many other cell types essential to the vertebrate body.-"In early blastula embryos, pluripotent cells were thought to exist only transiently; as an embryo develops, cells become restricted into categories of cells called germ layers and then into specialized cell types. The Northwestern study suggests that not all cells get restricted at those early stages. Instead, neural crest cells may have evolved as a consequence of a subset of blastula cells retaining activity of the regulatory network underlying pluripotency.-" The study underscores just how much remains to be discovered about embryonic development. The human body has more than 10 trillion cells elaborately organized into tissues and organs that are intricate and highly complex, yet it all is self-assembled from a single cell, the fertilized egg."

Genome complexity in embryology: neural crest cells

by Balance_Maintained @, U.S.A., Wednesday, May 06, 2015, 19:49 (3250 days ago) @ David Turell

We can't get 5 conscious humans to self-assemble and work together in complex intricate ways without prior planning and possible threats of bodily harm, yet 10 trillion cells did it randomly...... I think not.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity in embryology: neural crest cells

by dhw, Wednesday, May 06, 2015, 21:43 (3250 days ago) @ David Turell

DAVID: More and more complexity. Pluripotential neural crest cells:-http://www.sciencedaily.com/releases/2015/04/150430145125.htm
 
"'Neural crest cells never had their potential restricted at all," LaBonne said. "We believe a small population of early stem cells were set aside, so that when the time came, their immense developmental potential could be unleashed to create new features characteristic of vertebrates."-I like the sound of these. Cells of unlimited potential that can fit into new combinations, fulfilling new functions. Under "Hunter questions" you wrote: "An absolutely logical set of reasons why random mutation cannot work. So we are back to an IM or direct guidance. And I must insist with this set of reasons the IM must have guidance." I don't know why you must insist that your God is not clever enough to invent a mechanism that can work things out for itself. We have talked ad nauseam about how this "guidance" works: preplanned 3.7 billion years ago, or every single process and innovation specially supervised on the spot, presumably with several organisms at a time, since one wouldn't be enough. But you don't like to discuss that. Well, I "must insist" that an autonomous inventive mechanism that enables cells to create new combinations and functions remains a reasonable proposition. My little hypothesis extends a warm welcome to neural crest cells.

Genome complexity in embryology: neural crest cells

by David Turell @, Wednesday, May 06, 2015, 21:53 (3250 days ago) @ dhw


> "'Neural crest cells never had their potential restricted at all," LaBonne said. "We believe a small population of early stem cells were set aside, so that when the time came, their immense developmental potential could be unleashed to create new features characteristic of vertebrates."
> 
> I like the sound of these. Cells of unlimited potential that can fit into new combinations, fulfilling new functions....I don't know why you must insist that your God is not clever enough to invent a mechanism that can work things out for itself.-Because a fully autonomous mechanism might take off in tangents that outside the bounds of what God wants. If God implanted guidance paths, then we are back to semiautonomous.-> dhw: Well, I "must insist" that an autonomous inventive mechanism that enables cells to create new combinations and functions remains a reasonable proposition. My little hypothesis extends a warm welcome to neural crest cells.-What is really amazing is one little fertilized egg makes a human with 10 trillion well-organized cells, with each cell type doing something different than the others, all through embryologic development.

Genome complexity: many proteins from a few genes

by David Turell @, Thursday, February 11, 2016, 20:58 (2969 days ago) @ David Turell

We have 20,000genes and 100,000 proteins in our bodies. How is that?:-http://medicalxpress.com/news/2016-02-alternative-proteins-encoded-gene-widely.html-" For one, it may help explain how the mere 20,000 protein-coding genes in the human genome - fewer than are found in the genome of a grape—can give rise to creatures of such enormous complexity. Scientists know that the number of different proteins in human cells, thought to be upwards of 100,000, far exceeds the number of genes, but many questions have remained. Do most of those proteins have a unique function in the cell, or do their roles sometimes overlap? The discovery that different protein isoforms encoded by the same gene may have divergent functions on a larger scale than realized suggests that they vastly multiply what our genes are capable of.-***-"One of the ways that cells produce multiple protein isoforms from individual genes is a process called alternative splicing. Most human genes contain multiple segments called exons, separated by intervening non-coding sequences called introns. In the cell, different combinations of these individual exons are "glued" or spliced together to generate a final expressed gene product; thus, a single gene can encode a set of distinct, but related protein isoforms, depending on the specific exons that are spliced. One isoform, for example, may result from splicing exons A-B-C-D of a particular gene. Another may arise from the skipping of exon C, resulting in a product with only exons A-B-D.-***-"Of the roughly 20,000 genes in the human genome that code for proteins, researchers concentrated on about eight percent. Using ORF-Seq, they ultimately created a collection of 1,423 protein isoforms for 506 genes, of which more than 50 percent were entirely novel gene products. They subjected 1,035 of these protein isoforms through a mass screening test that paired them with 15,000 human proteins to see which would interact.-"'The exciting discovery was that isoforms coming from the same gene often interacted with different protein partners," remarked Gloria Sheynkman, PhD, of Dana-Farber and one of the lead authors. "This suggests that the isoforms play very different roles within the cell" - much as siblings with different careers often interact with different sets of friends and co-workers.-"The researchers found that in most cases, related isoforms shared less than half of their protein partners. Sixteen percent of related isoforms share absolutely no protein partners. "From the perspective of all the protein interactions within a cell, related isoforms behave more like distinct proteins than minor variants of one another.-***-"Intriguingly, isoforms that stem from a minuscule difference in DNA - a difference of just one letter of the genetic code—sometimes had starkly different roles within the cell, researchers found. At the same time, related isoforms that are structurally quite different may have very similar roles.-"Quite often, the interaction partners of related isoforms vary from tissue to tissue, the researchers found. In the liver, for example, an isoform may interact with one set of proteins. In the brain, a relative of that isoform may interact with a largely different set of protein partners."-Comment: And all of this process is in the non-coding part of DNA, the so-called 'junk' part. Too complex for chance.

Genome complexity: enzymes help repair DNA

by David Turell @, Friday, February 12, 2016, 20:19 (2968 days ago) @ David Turell

A system of enzymes has been found which appears to help repair damaged DNA by methylation:-http://www.sciencedaily.com/releases/2016/02/160212102340.htm-"A team of scientists in Japan has found that a DNA modification called 5hmC -- thought to be involved in turning genes on and off -- localizes at sites of DNA damage and repair. They also found that a family of recently discovered enzymes, called TETs for short, is important in maintaining 5hmC's reparative role.-"To turn genes on or off, a methyl group can be added to or removed from DNA. During the removal of this chemical tag, called demethylation, the methyl group is converted to 5hmC as an intermediate step. The TET enzymes are thought to be critical to the demethylation process. Recent research has shown that 5hmC is associated with an "opening up" of nearby chromatin, the tightly packaged assembly of proteins and DNA in the cell nucleus.-"The team reveals in the journal Cell Reports that 5hmC localizes near breaks in DNA that develop naturally or that are caused by DNA-damaging drugs or irradiation. They also found that inhibiting TET enzymes in cells resulted in a lack of 5hmC, followed by errors in chromosome separation. This suggests that TET enzymes are important for the production of 5hmC at DNA damage sites and that both play critical roles in responding to DNA damage.-"The research raises the possibility that 5hmC helps to keep chromatin "open" so it can be more accessible to other DNA damage response proteins. 5hmC could be used as a marker for DNA damage, say the researchers.-"'Our results imply that loss of TET enzymes and 5hmC depletion could contribute significantly to genome instability and inaccurate chromosome segregation, perhaps explaining the correlation of low 5hmC levels with cancer," say the researchers."-Comment: Here evolution came up with two enzymes, which are giant specialized molecules, to help repair DNA. How did undirected evolution do that discovery?

Genome complexity: RNA has an extra letter!

by David Turell @, Wednesday, February 17, 2016, 06:01 (2963 days ago) @ David Turell

RNA does the translation of DNA code and modifies gene expression. a new letter for the code has been found:-https://www.sciencedaily.com/releases/2016/02/160216181447.htm-"DNA, RNA, protein -- the end. Or is it? Until recently, the pattern used to encode genetic information into our cells was considered to be relatively straightforward: four letters (A,G,C,T) for DNA and four (A,G,C,U) for RNA. -***-"The number of modified nucleotides (letters) in RNA is 10 times larger than that of the letters found in DNA. But what accounts for the evolutionary drive for a large RNA alphabet? RNA molecules have a wide variety of functions, including storage of genetic information as well as catalytic, structural, and regulatory activities. This is in contrast to the important but one-dimensional function of DNA in encoding genetic information.-"'The 140 or so different modifications that decorate RNA increase significantly the vocabulary of RNA and enable the various types of RNA, including mRNA, rRNA, tRNA, siRNA, miRNA and, lncRNA, to implement their versatile activities," said Prof. Rechavi.-"Prof. Rechavi's group, led by Dan Dominissini and Sharon Moshkovitz, began exploring the landscape of chemical modifications of messenger RNA (mRNA) four years ago through a specific modification: the addition of a methyl group in position 6 of Adenosine (m6A) in mRNA. The research team then showed that this modification is specific to unique regions of the mRNA molecules and that the modification can be "read" by specific proteins. They also showed that this modification is dynamic and responds to environmental stimuli.-"These findings complemented the identification by Prof. He's University of Chicago group at the time of an enzyme (FTO) that removes the m6A marks from mRNA. The demonstration of a reversible process that decorates mRNA and affects its stability, translatability, splicing, and localization established a new field of RNA "epigenetics" known as "epitranscriptomics-"In their new study, the researchers unraveled a new dynamic modification of mRNA -- the methylation of position 1 of Adenosine (m1A). Importantly, this modification was shown to be localized in a telltale position near the start of protein translation and linked to increased protein synthesis. Thousands of genes are decorated by this modification, allowing cells to regulate the expression of proteins needed for key biological processes."-Comment: Ever more complexity. It shows how 20,000+ genes make a complex human. How much complexity is needed before it is so complex it must be considered designed? With research it will only be shown to much more complex. Design?

Genome complexity: Plants have memories

by David Turell @, Monday, February 22, 2016, 16:00 (2958 days ago) @ David Turell

Plans can develop memories of how to handle a drought, and also lose those memories:-http://phys.org/news/2016-02-memories.html-"A small team of researchers with Australian National University Canberra, has found evidence that suggests that plants are able to reset a memory that has not been proven to be useful, in essence, forgetting things after they have been stored.-***-"Prior research has shown that plants are able to 'remember' events such as droughts, so they will not have to go through the same process of learning to survive under such conditions if another drought occurs. Other studies have shown that the process involves DNA, because some plants are able to pass on such memories to their offspring—but how such memory passing was done was mostly unknown. In this new effort, the researchers report learning not only more about how such memory processing occurs, but also how plants are able to reset if conditions change such that a memory that has been learned that is no longer useful can be eliminated.-"The researchers found that in order for a plant to create a memory, it has to create a certain protein—one that will have an impact on its own DNA, which allows for impacting future generations. It is all part of a process called RNA decay, they report, where DNA strands are transcribed into RNA, before they are translated into proteins. It is the RNA decay process that controls the amount of RNA molecules that are to be tuned into proteins—any disruption to that process prevents a memory from being formed, they note, suggesting the means by which prior memories may be eliminated. Doing so is important , they add, because holding onto memories uses resources—if a plant seed is blown into an area where a drought will never occur, for example, than it should release the memory of how to contend with one, thus conserving its energy. ( my bold)-"The team notes too that some plants also appear to have a type of short-term memory that is not related to either DNA or RNA, but thus far it is not understood, primarily, because it has not yet been studied."-Comment: Shapiro and others would view this as plant mentation, extrapolating from his view of cells. I view it as a built-in biochemical response.

Genome complexity: cell splirtting DNA mechanics

by David Turell @, Thursday, February 25, 2016, 13:50 (2955 days ago) @ David Turell

Cells reproduce constantly by splitting in two. This requires unzipping DNA and making duplicate strands. The molecular machine that does this is called a helicase, and it walks along the DNA and rocks back and forth splitting. And it is and extremely complicated structure:-http://www.evolutionnews.org/2016/02/is_it_a_pumpjac102625.html-"One part binds and releases energy from a molecule called ATP. It converts the chemical energy into a mechanical force that changes the shape of the helicase," Li said. After kicking out the spent ATP, the helicase complex goes back to its original shape so a new ATP molecule can come in and start the process again.-"It looks and operates similar to an old style pumpjack oil rig, with one part of the protein complex forming a stable platform, and another part rocking back and forth," Li said. Each rocking motion could nudge the DNA strands apart and move the helicase along the double helix in a linear fashion, he suggested-The source article: -http://www.nature.com/nsmb/journal/vaop/ncurrent/full/nsmb.3170.html-(Look at the diagrams. Complex!)-Abstract: -"The CMG helicase is composed of Cdc45, Mcm2-7 and GINS. Here we report the structure of the Saccharomyces cerevisiae CMG, determined by cryo-EM at a resolution of 3.7-4.8 Å. The structure reveals that GINS and Cdc45 scaffold the N tier of the helicase while enabling motion of the AAA+ C tier. CMG exists in two alternating conformations, compact and extended, thus suggesting that the helicase moves like an inchworm. The N-terminal regions of Mcm2-7, braced by Cdc45-GINS, form a rigid platform upon which the AAA+ C domains make longitudinal motions, nodding up and down like an oil-rig pumpjack attached to a stable platform. The Mcm ring is remodeled in CMG relative to the inactive Mcm2-7 double hexamer. The Mcm5 winged-helix domain is inserted into the central channel, thus blocking entry of double-stranded DNA and supporting a steric-exclusion DNA-unwinding model.-***-"DNA replication is a major source of errors that can lead to cancer," explained Li, a Professor in the Department of Biochemistry & Cell Biology at Stony Brook University, a scientist at Brookhaven Lab, and lead author of the paper. "The entire genome -- all 46 chromosomes -- gets replicated every few hours in dividing human cells," Li said, "so studying the details of how this process works may help us understand how errors occur. -***-"Yet the machinery is much more rapid than the best typist. It rocks! -- not like the slow, lumbering mechanism of the oil pumpjack, but at blinding speed. Jonathan M. wrote here at Evolution News that DNA replication works at 749 bases per second with an error rate of 10-7 to 10-8. Yet the cell performs this feat in just hours, trillions of times in your body. Nor does it work alone. All the other machines in the DNA replication factory keep up with it, bringing in nucleotides, proofreading them, and fastening the new helices together."-Comment: Just one 'simple' part of how living things thrive. Not by chance!

Genome complexity: retroviruses conrol immunity

by David Turell @, Friday, March 04, 2016, 15:22 (2947 days ago) @ David Turell

DNA has about 8% retrovirus remnants which can control interferon usage, a basic defense mechanism:-http://www.the-scientist.com/?articles.view/articleNo/45503/title/Viral-Remnants-Help-Regulate-Human-Immunity/&utm_campaign=NEWSLETTER_TS_The-Scientist-Daily_2016&utm_source=hs_email&utm_medium=email&utm_content=26940621&_hsenc=p2ANqtz-8rYpCVdLFk4R8-_AQET5OIVkXV8aZrDQuXcjyglie1-tV0N4hqyvSpbRjJ9mvMsT8b8hYTG1C785ZM_AFIkmeAdrWvPg&_hsmi=26940621/-"Remnants of retroviruses that entered the human genome millions of years ago can regulate some innate immune responses. These viral sequences have previously been linked to controlling early mammalian development and formation of the placenta, among other things. A study published today (March 3) in Science establishes that one such endogenous retrovirus in human cells can also regulate the interferon response, which helps organisms quickly respond to infections. The work is one of the first reports to show that human cells could have adopted retroviral sequences to regulate their genes.-***-"Chuong and his University of Utah mentors Nels Elde and Cédric Feschotte began by scanning the sequences around interferon-induced genes, finding at least 27 transposable elements that likely originated from the long repeats at the ends of retroviral sequences. One such element, known as MER41, comes from a virus that invaded the genome approximately 45 million to 60 million years ago; the team found that its sequence in present-day human cells contained interferon-inducible binding sites.-"The group then focused on a MER41 sequence that occurs 220 base pairs upstream of an interferon-induced gene called AIM2, which activates an inflammatory response in cells. When the researchers deleted this MER41 element in a cell line using CRISPR/Cas9 gene editing, interferon treatment could not trigger the AIM2 gene. Without the interferon-mediated response, these cells were more susceptible to viral infections, the team found.-***-"In addition to AIM2, the group found MER41 elements helped regulate at least three other interferon-inducible genes involved in human immunity. Looking across the genomes of other mammals, the researchers also found MER41-like regulatory elements in lemurs, bats, and other species.-***-"Whether host cells coopted the viral sequences for their regulatory needs or if ancient viruses used their regulatory abilities to control host immunity during invasion is still unknown, according to Feschotte. “We can only speculate why ancient viruses might have carried these regulatory switches to begin with, but data suggest they had these systems built into their sequence already,” he told The Scientist. (my bold)-"Endogenous retroviral elements make up about 8 percent of the human genome, and similar regulatory effects might be found on other mammalian gene functions, said Mager. “What's cool about endogenous retroviruses is that their ends, known as LTRs, are optimized to have all these regulatory sequences in just 300 to 400 base pairs of DNA,” she said. “These units are powerhouses of regulatory potential.'”-Comment: Note my bold. Is this pre-planning using viruses to build effective DNA defenses?

Genome complexity: in embryology

by David Turell @, Thursday, March 24, 2016, 22:21 (2927 days ago) @ David Turell

By the time the embryo is only four cells old, the cells are differentiating:-https://www.sciencedaily.com/releases/2016/03/160324142932.htm-"Once an egg has been fertilised by a sperm, it divides several times, becoming a large free-floating ball of stem cells. At first, these stem cells are 'totipotent', the state at which a stem cell can divide and grow and produce everything--every single cell of the whole body and the placenta, to attach the embryo to the mother's womb. The stem cells then change to a 'pluripotent' state, in which their development is restricted to generating the cells of the whole body, but not the placenta. However, the point during development at which cells begin to show a preference for becoming a specific cell type is unclear.-"Now, in a study published in the journal Cell, scientists at the University of Cambridge and the European Bioinformatics Institute (EMBL-EBI) suggests that as early as the four-cell embryo stage, the cells are indeed different.-***-"They showed that some genes in each of the four cells behaved differently. The activity of one gene in particular, Sox21, differed the most between cells; this gene forms part of the 'pluripotency network'. The team found when this gene's activity was reduced, the activity of a master regulator that directs cells to develop into the placenta increased.-***-"'We now know that even as early as the four-stage embryo - just two days after fertilisation - the embryo is being guided in a particular direction and its cells are no longer identical.'"-Comment: Genes turn on and off in embryology to create proper form under a master plan in the DNA, so they are not just making proteins. The activity has to be automatic to create the necessary result. Mistakes can make terrible anomalies.

Genome complexity: role of lncRna's

by David Turell @, Friday, April 08, 2016, 16:05 (2912 days ago) @ David Turell

Long non-coding RNA sect1ons of DNA may have an enhancer role for gene activity:-https://www.sciencedaily.com/releases/2016/04/160407150730.htm-"A new genetic clue discovered by a team co-led by a researcher at the Perelman School of Medicine at the University of Pennsylvania is shedding light on the functions of the mysterious "long non-coding RNAs" (lncRNAs). These molecules are transcribed from genes and are often abundant in cells, yet they do not code for proteins. Their functions have been almost entirely unknown--and in recent years have attracted much research and debate.-***-"Some non-protein-coding genes produce small RNA molecules, and many of these have known functions, often in regulating other genes or RNAs. But thousands of our genes produce lncRNAs--defined as being at least 200 nucleotides in length--and their functions remain poorly understood.-"In a study published in 2014, Paralkar and colleagues identified over a thousand distinct lncRNAs in mouse and human blood cells. Most had never been described before. But many turned out to originate from areas of the genome containing known or suspected enhancers--small regions of DNA where transcription factor molecules gather, to stimulate the transcription of nearby genes.-***-"The researchers found strong evidence that in the twisted, looping, double-helix structure of the genome, the promoter end of Lockd DNA comes into direct physical contact with the promoter end of its neighbor Cdkn1b, and in that way acts as an enhancer to stimulate Cdkn1b's transcription.-"Paralkar acknowledged that the Lockd RNA may one day be found to have some other function. "It's impossible to prove absolutely that it has no function--but it seems at least that it has no obvious function in regulating its neighbor Cdkn1b," he said. He emphasized, however, that in determining the function of non-coding DNA and RNA, both DNA-deletion and RNA-blocking experiments--as in this study--are needed to distinguish the function of DNA from its RNA product.-"'One has to decouple the transcript from the DNA," Paralkar said. "Future studies of lncRNA function should adhere to that requirement."-"He added that the discovery of this enhancer function for one example of a lncRNA gene points to the possibility that this is a broadly used mechanism in the genome, found in non-coding and perhaps even some protein-coding genes. Indeed, enhancers are theorized to be one of the key genomic features that distinguishes species such as mice and humans--which share nearly all their protein-coding genes, but relatively few of their enhancers and lncRNA-coding genes.-"'The fact that mice and humans are so different may be due largely to the fact that their genes are being regulated so differently by enhancers, some of which produce RNA molecules that we detect as lncRNAs," Paralkar said."-Comment: Less and less junk DNA. Again a pattern of basic DNA for all animals with modifiers added for different species, simplifying how evolution can be programmed for more complexity as it advances. All fits into my theories.

Genome complexity: mechanism stopped evolving

by David Turell @, Friday, May 06, 2016, 15:05 (2884 days ago) @ David Turell

The general pattern of how the genome works was established at the beginning of life and stopped changing more than 3 billion yeas ago:-http://motherboard.vice.com/read/why-did-the-genetic-code-of-all-life-on-earth-suddenly-stop-evolving-"All life on Earth exists thanks to a universal genetic code. This biological rulebook tells our cells how DNA should be translated into life-supporting proteins, without which we couldn't survive. -"Even though the genetic code commands a seemingly immeasurable number of organisms, it also binds us all together as descendents of a shared ancestor—a lingua franca for life.-"Yet for all of its diverse and essential properties, the genetic code is static. For some reason unknown to scientists, approximately 3 billion years ago it simply stopped growing. Instead of expanding to encode new combinations of amino acids, and potentially new life, it stagnated at its current size and function. But a new study published today in the journal Science Advances offers an explanation for the genetic code's mysterious evolutionary limit.-"A team of geneticists discovered that several billion years ago, the genetic code reached a point of self-preservation. Namely, it could continue evolving and risk mutating the building blocks of life it was responsible for creating, or it could remain limited, albeit functional.-***-"Over millennia, the genetic code evolved to contain “codons” of three nucleotides, which transfer RNA (tRNA) translate into a 20-letter chain of amino acids, leading to the creation of basic proteins. However, at some point in history, transfer RNA hit a functional limit to the number of amino acids it was able to successfully interpret into proteins, the study found. It was at that point the genetic code, and the complexity of organic life, stood relatively still.-"Any more than 20 amino acids, and the machinery of gene expression got confused. The results of such erroneous translation were constant mutations "with catastrophic consequences,” according to Ribas.-"While the expansion of the genetic code allowed for new tRNA creation, the particular L-shaped cavity of ribosomes—the part of the cell where protein is actually constructed—ultimately allowed for very little variation. If tRNA molecules didn't adapt to accommodate the specific needs of the ribosome, the efficiency of protein synthesis would be vastly compromised, and fatal for life.-“'There came a point when nature was unable to create new tRNAs that differed sufficiently from those already available without causing a problem with the identification of the correct amino acid. And this happened when 20 amino acids were reached,” Ribas explained."-Comment: The genome reached a practical limit to its complexity, is a reasonable explanation. That all life uses the same system means evolution was organized from the beginning by starting at one point. God's management is suggested.

Genome complexity: mutations self-directed?

by David Turell @, Friday, May 06, 2016, 15:22 (2884 days ago) @ David Turell

That is what is suggested by this article:-http://toddcwood.blogspot.ca/2016/05/research-week-directed-mutations.html- " Pinto et al. looked at an enzyme called APOBEC3G, that is part of a family of genes in human and ape genomes that deaminate cytosines. "Deaminating cytosine" is a sort of "directed mutation," because that chemical reaction changes the sequence of DNA at a single nucleotide position. - "APOBEC enzymes are thought to defend human cells against viruses by mutating them so they don't work any more. Pinto et al. wondered if there might be evidence of APOBEC enzymes acting on human and ape genomes as well. Think of it as a sort of "collateral damage" in the war against viruses. In their survey, they found eight thousand unique clusters of mutations that look like APOBEC mutations in the human genome, as well as the genomes of Neandertal and Denisovans. They found almost a half million that were unique to the entire genus Homo. The fact that these mutations are unique to these different forms of human indicates that this enzyme has indeed altered human genome sequences since creation. And that's just one version of an enzyme family that has multiple variants in the human genome.-" Now, we have to put this into perspective. APOBEC doesn't account for all variations in the human genome, or even most of the variations. It doesn't explain why the human genome is nearly identical to other ape genomes. All we get from this research is one example of how an enzyme really could alter a human genome sequence at one nucleotide position. That's pretty exciting stuff, though, and it greatly alleviates my unease about "directed mutations." They really can happen."-Comment: this is part of the immune system defenses. We develop a system of memory cells (T cells, B cells in lymphocytes) with modified DNA which gives us the output of antibodies against infections of all sorts and most of thee memories last a lifetime. This is a purposeful mechanism against infections, resembles epigenetics but isn't as a valid part of the initial genome.

Genome complexity: mechanism stopped evolving

by dhw, Saturday, May 07, 2016, 11:43 (2883 days ago) @ David Turell

David's comment: The genome reached a practical limit to its complexity, is a reasonable explanation. That all life uses the same system means evolution was organized from the beginning by starting at one point. God's management is suggested.
-Why “organized”? That all life uses the same system is the very essence of common descent. The starting point may have been managed by your God, but higgledy-piggledy, unorganized evolution would also have started at that point.

Genome complexity: mechanism stopped evolving

by David Turell @, Saturday, May 07, 2016, 15:15 (2883 days ago) @ dhw

David's comment: The genome reached a practical limit to its complexity, is a reasonable explanation. That all life uses the same system means evolution was organized from the beginning by starting at one point. God's management is suggested.
> 
> 
> dhw: Why “organized”? That all life uses the same system is the very essence of common descent. The starting point may have been managed by your God, but higgledy-piggledy, unorganized evolution would also have started at that point.-You assume the standard form of DNA just appeared out of no where. Once again you are avoiding the absolute connectivity of origin of life and evolution. If DNA is present it had to be created by chance or design, no third way.

Genome complexity: mechanism stopped evolving

by dhw, Sunday, May 08, 2016, 13:05 (2882 days ago) @ David Turell

David's comment: The genome reached a practical limit to its complexity, is a reasonable explanation. That all life uses the same system means evolution was organized from the beginning by starting at one point. God's management is suggested.-dhw: Why “organized”? That all life uses the same system is the very essence of common descent. The starting point may have been managed by your God, but higgledy-piggledy, unorganized evolution would also have started at that point.-DAVID: You assume the standard form of DNA just appeared out of no where. Once again you are avoiding the absolute connectivity of origin of life and evolution. If DNA is present it had to be created by chance or design, no third way.-Once again you are switching the argument from evolution (Chapter 2) to origins (Chapter 1). Even bacteria have DNA. You quote me and then ignore my quote: “The starting point may have been managed by your God.” The disagreement between us concerns whether your God planned every step of evolution, or left his invention to pursue its own course.

Genome complexity: mechanism stopped evolving

by David Turell @, Sunday, May 08, 2016, 15:34 (2882 days ago) @ dhw


> dhw: Once again you are switching the argument from evolution (Chapter 2) to origins (Chapter 1). Even bacteria have DNA. You quote me and then ignore my quote: “The starting point may have been managed by your God.” The disagreement between us concerns whether your God planned every step of evolution, or left his invention to pursue its own course.-Sorry, but you cannot ignore origin is a continuum to life now. You like your discontinuity, because it allows you to separate arguments into parts when they are not separate. You don't accept God started life, but are willing to entertain it is a possibility. You don't accept humans as a desired conclusion. I do. We are still debating across a large gulf.

Genome complexity: mechanism stopped evolving

by dhw, Monday, May 09, 2016, 13:18 (2881 days ago) @ David Turell

dhw: Once again you are switching the argument from evolution (Chapter 2) to origins (Chapter 1). Even bacteria have DNA. You quote me and then ignore my quote: “The starting point may have been managed by your God.” The disagreement between us concerns whether your God planned every step of evolution, or left his invention to pursue its own course.-DAVID: Sorry, but you cannot ignore origin is a continuum to life now. You like your discontinuity, because it allows you to separate arguments into parts when they are not separate. You don't accept God started life, but are willing to entertain it is a possibility. You don't accept humans as a desired conclusion. I do. We are still debating across a large gulf.-If I accept the possibility of your God starting life and evolution, I can hardly be accused of ignoring origins. I'm afraid I can't see discontinuity in my arguments (though that is the very fault I find with your own, as you struggle to link your anthropocentrism to the rest of evolution's history). Here are the facts as we know them: life started, vast numbers of organisms evolved through vast numbers of innovations, most died out but humans are here, along with the duck-billed platypus, the weaverbird's nest, and my dear friends the ants. There are various ways in which these facts can be linked in a pattern. You have offered one, and I have offered an alternative which seems to me to bind all these sections together.-Under “Cosmologic Philosophy” (thank you again) you quote the following:
"Perhaps it isn't possible for the intellect to overcome a sense of the arbitrariness of things. We are close here to the old philosophical riddle, of why there is something rather than nothing. That's a mystery into which perhaps no light can penetrate."
Your comment: Note, no explanation for why things are the way they are.-Exactly. We can only speculate, draw our different patterns, and see how far they do or do not fit the facts as we observe them. I point out the gaps in yours, and you point out the gaps in mine. New facts are coming to light all the time - and you do a fantastic job in keeping us informed of them. It seems that the more facts we learn, the less clear the overall picture becomes, but on we go. Endlessly fascinating…and a tribute to the indomitability of the human spirit.

Genome complexity: mechanism stopped evolving

by David Turell @, Monday, May 09, 2016, 19:20 (2881 days ago) @ dhw


> dhw:If I accept the possibility of your God starting life and evolution, I can hardly be accused of ignoring origins. ...Here are the facts as we know them: life started, vast numbers of organisms evolved through vast numbers of innovations, most died out but humans are here, along with the duck-billed platypus, the weaverbird's nest, and my dear friends the ants. There are various ways in which these facts can be linked in a pattern. You have offered one, and I have offered an alternative which seems to me to bind all these sections together.-I'm pointing out one aspect of your narrative: first life started with an early genome (DNA plus modifying parts) at time zero. It is still here. Continuum. The rest is talk around the issue. I know Darwin skipped origin and yes evolution follows, but there is no gap in the presence of the genome.. Continuum. All discussion must cover all of the continuum.
 
> dhw: Your comment: Note, no explanation for why things are the way they are.
> 
> Exactly. We can only speculate, draw our different patterns, and see how far they do or do not fit the facts as we observe them. I point out the gaps in yours, and you point out the gaps in mine. New facts are coming to light all the time - and you do a fantastic job in keeping us informed of them. It seems that the more facts we learn, the less clear the overall picture becomes, but on we go. Endlessly fascinating…and a tribute to the indomitability of the human spirit.-Thank you and things become more and more clear to me. I'm sorry for your fuzziness.

Genome complexity: mechanism stopped evolving

by dhw, Tuesday, May 10, 2016, 16:50 (2880 days ago) @ David Turell

dhw:If I accept the possibility of your God starting life and evolution, I can hardly be accused of ignoring origins. ...Here are the facts as we know them: life started, vast numbers of organisms evolved through vast numbers of innovations, most died out but humans are here, along with the duck-billed platypus, the weaverbird's nest, and my dear friends the ants. There are various ways in which these facts can be linked in a pattern. You have offered one, and I have offered an alternative which seems to me to bind all these sections together.-DAVID: I'm pointing out one aspect of your narrative: first life started with an early genome (DNA plus modifying parts) at time zero. It is still here. Continuum. The rest is talk around the issue. I know Darwin skipped origin and yes evolution follows, but there is no gap in the presence of the genome.. Continuum. All discussion must cover all of the continuum.-What is “the” issue? Here is a theistic continuum: God created life, the genome and whatever other mechanism was necessary for organisms to evolve; vast numbers of organisms evolved etc.…(see bold above for the rest). One pattern: God left the mechanism to follow its own course (perhaps with the occasional dabble), which is why we have the higgledy-piggledy history of evolution, with 99% of species disappearing, weaverbirds building complicated nests, bugs lodging in carnivorous plants, and crocodiles having special vision. Another pattern: God planned and guided the 99% disappearance, the nest, the bugs and the crocky eyes because they were essential to the balance of nature, so that he could fulfil his purpose of producing and feeding humans.
 
DAVID: […] things become more and more clear to me. I'm sorry for your fuzziness.
-Strange. I find the first pattern somewhat less fuzzy than the second.

Genome complexity: mechanism stopped evolving

by David Turell @, Tuesday, May 10, 2016, 18:11 (2880 days ago) @ dhw


> DAVID: […] things become more and more clear to me. I'm sorry for your fuzziness.
> 
> 
> dhw: Strange. I find the first pattern somewhat less fuzzy than the second.-And I still think God would not have bothered with all this without keeping an eye on it to be sure it worked out like He intended. All inventors have purposes in mind.

Genome complexity: mechanism stopped evolving

by BBella @, Tuesday, May 10, 2016, 19:32 (2880 days ago) @ David Turell


> > DAVID: […] things become more and more clear to me. I'm sorry for your fuzziness.
> > 
> > 
> > dhw: Strange. I find the first pattern somewhat less fuzzy than the second.
> 
> And I still think God would not have bothered with all this without keeping an eye on it to be sure it worked out like He intended. All inventors have purposes in mind.-But God would not be your common inventor as we know inventors to be. It seems to me, if there were an all wise God, who in the beginning created all that IS and then rested from his works and let be, as the scriptures testify, I would think that kind of God would have no need to fiddle, as he would have already implanted every need, variation and ability needed into All That IS. Not to say, as the scriptures also testify, he didn't fiddle with the plans of man. -But as you know, if there was A God in the beginning, what I think is more likely the case, God multiplied and became ALL That IS which explains why ATI is so brilliant! And that simply explains everything except how.

Genome complexity: mechanism stopped evolving

by David Turell @, Tuesday, May 10, 2016, 21:56 (2880 days ago) @ BBella


> Bbella: But as you know, if there was A God in the beginning, what I think is more likely the case, God multiplied and became ALL That IS which explains why ATI is so brilliant! And that simply explains everything except how. - As before, I compare your idea with my universal consciousness as being very close ideas, as a UI will encompass everything.

Genome complexity: mechanism stopped evolving

by dhw, Wednesday, May 11, 2016, 12:50 (2879 days ago) @ BBella

DAVID: […] things become more and more clear to me. I'm sorry for your fuzziness.
dhw: Strange. I find the first pattern somewhat less fuzzy than the second.-DAVID: And I still think God would not have bothered with all this without keeping an eye on it to be sure it worked out like He intended. All inventors have purposes in mind.-I had suggested he kept an eye on it because maybe he invented it precisely in order to keep an eye on it - i.e. as the hidden audience, the intention being an enjoyably unpredictable spectacle (see below), though he could always step in. You agree that he's hidden, but you don't like him being an audience - he apparently wants a relationship and that, mysteriously, is why he hides.-BBELLA: But God would not be your common inventor as we know inventors to be. It seems to me, if there were an all wise God, who in the beginning created all that IS and then rested from his works and let be, as the scriptures testify, I would think that kind of God would have no need to fiddle, as he would have already implanted every need, variation and ability needed into All That IS. Not to say, as the scriptures also testify, he didn't fiddle with the plans of man.-Maybe he's not all wise. Maybe he's a process God, learning as he goes. Wouldn't it be incredibly boring to know everything? Do you enjoy novels, plays, films whose plot developments and denouement are already obvious from the start?-BBELLA: But as you know, if there was A God in the beginning, what I think is more likely the case, God multiplied and became ALL That IS which explains why ATI is so brilliant! And that simply explains everything except how.-Or maybe there was just energy in the beginning, and energy kept and keeps transforming itself into all the forms we know and don't know, some of them conscious, some of them not. And that would explain why ATI is such a rich mystery, and why we spend so much time vainly trying to grasp the ungraspable.

Genome complexity: mechanism stopped evolving

by David Turell @, Wednesday, May 11, 2016, 15:02 (2879 days ago) @ dhw


> DAVID: And I still think God would not have bothered with all this without keeping an eye on it to be sure it worked out like He intended. All inventors have purposes in mind.
> 
> dhw: I had suggested he kept an eye on it because maybe he invented it precisely in order to keep an eye on it - i.e. as the hidden audience, the intention being an enjoyably unpredictable spectacle (see below), though he could always step in. You agree that he's hidden, but you don't like him being an audience - he apparently wants a relationship and that, mysteriously, is why he hides.-Spoken like a playwright. What you miss is the obvious requirement of faith, the reason He stays hidden.-> dhw: Maybe he's not all wise. Maybe he's a process God, learning as he goes. Wouldn't it be incredibly boring to know everything? Do you enjoy novels, plays, films whose plot developments and denouement are already obvious from the start?-Again, the playwright in action. I don't believe true process theology takes that specific viewpoint.
> 
> BBELLA: But as you know, if there was A God in the beginning, what I think is more likely the case, God multiplied and became ALL That IS which explains why ATI is so brilliant! And that simply explains everything except how.
> 
> dhw: Or maybe there was just energy in the beginning, and energy kept and keeps transforming itself into all the forms we know and don't know, some of them conscious, some of them not. And that would explain why ATI is such a rich mystery, and why we spend so much time vainly trying to grasp the ungraspable.-Your supposition sounds just like conscious energy from the beginning, not requiring much transformation to accomplish goals!

Genome complexity: mechanism stopped evolving

by BBella @, Wednesday, May 11, 2016, 20:45 (2879 days ago) @ David Turell


> > dhw: I had suggested he kept an eye on it because maybe he invented it precisely in order to keep an eye on it - i.e. as the hidden audience, the intention being an enjoyably unpredictable spectacle (see below), though he could always step in. You agree that he's hidden, but you don't like him being an audience - he apparently wants a relationship and that, mysteriously, is why he hides.
> 
> Spoken like a playwright. What you miss is the obvious requirement of faith, the reason He stays hidden.-In the bible story, God spoke directly to his creation and so no requirement of faith/belief was required from him. Then God stopped speaking to man and then angels showed up and began speaking to them relaying Gods message (why God have to rely on angels? why couldnt he still speak to them himself?). Then they too disappeared. Then when they left, in comes Jesus (supposedly God in physicality on earth - though he never claimed to be God himself). Jesus spoke directly to his followers, so faith in a mysterious unseen God was not required then as well - only that they have faith/belief that he was who he said he was. So, according to the scriptures, God has not require faith/belief in a mysterious unseen figure. But, of course, anyone can choose to believe in an unseen figure as God. But think of the story flow here. God first speaks directly to them - altho they never seen him face to face, only heard his voice. Moses is the only one that supposedly seen him face to face, yet that is disputable, since the scriptures also says no "man" has ever seen God. So first they can hear his voice, then he sends representatives, then his son appears- then he disappears and now we have no one but our belief that there is someone out there that calls himself God. Definitely sounds to me closer to humans antics and less like an all powerful limitless being that created all that is. So if the first God, then his angels, then his son werent humans and doesnt sound like an all powerful creator God - what were they? The plot thickens: In walks the alien that fits neatly and perfectly into this scenario. What if I am right? Have you ever asked yourselves that?
 
> 
> > dhw: Maybe he's not all wise. Maybe he's a process God, learning as he goes. Wouldn't it be incredibly boring to know everything? Do you enjoy novels, plays, films whose plot developments and denouement are already obvious from the start?
> 
> Again, the playwright in action. I don't believe true process theology takes that specific viewpoint.-Yes, that is exactly how process theology goes.-> > dhw: Or maybe there was just energy in the beginning, and energy kept and keeps transforming itself into all the forms we know and don't know, some of them conscious, some of them not. And that would explain why ATI is such a rich mystery, and why we spend so much time vainly trying to grasp the ungraspable.
> 
> Your supposition sounds just like conscious energy from the beginning, not requiring much transformation to accomplish goals!-But he said some of the forms are conscious and some are not. If conscious energy is what was from/in the beginning, then how can there be unconscious forms? From what would conscious energy form the unconscious form from?

Genome complexity: mechanism stopped evolving

by David Turell @, Thursday, May 12, 2016, 00:46 (2879 days ago) @ BBella

Bbella: In the bible story, God spoke directly to his creation and so no requirement of faith/belief was required from him..... So if the first God, then his angels, then his son werent humans and doesnt sound like an all powerful creator God - what were they? The plot thickens: In walks the alien that fits neatly and perfectly into this scenario. What if I am right? Have you ever asked yourselves that?-No, I haven't thought about aliens. And since I accept the OT as partially covering the true history of the Hebrews but not the fanciful stories (i.e., Jonah in the whale) and since I see God as hidden now, I have no problem with my statement that God is concealed and requires faith.
> > 
> > David Again, the playwright in action. I don't believe true process theology takes that specific viewpoint.
> 
> Bbella: Yes, that is exactly how process theology goes.-Thank you for educating me. I was unclear on the point, not having closely studied it.
> 
> > > dhw: Or maybe there was just energy in the beginning, and energy kept and keeps transforming itself into all the forms we know and don't know, some of them conscious, some of them not. And that would explain why ATI is such a rich mystery, and why we spend so much time vainly trying to grasp the ungraspable.
> > 
> > David: Your supposition sounds just like conscious energy from the beginning, not requiring much transformation to accomplish goals!
> 
> BBella: But he said some of the forms are conscious and some are not. If conscious energy is what was from/in the beginning, then how can there be unconscious forms? From what would conscious energy form the unconscious form from?-I simply think all eternal energy was conscious. I don't think consciousness can appear de novo from nothing. The original energy was conscious.

Genome complexity: mechanism stopped evolving

by BBella @, Thursday, May 12, 2016, 22:16 (2878 days ago) @ David Turell

dhw: Or maybe there was just energy in the beginning, and energy kept and keeps transforming itself into all the forms we know and don't know, some of them conscious, some of them not. And that would explain why ATI is such a rich mystery, and why we spend so much time vainly trying to grasp the ungraspable.
> > > 
> > > David: Your supposition sounds just like conscious energy from the beginning, not requiring much transformation to accomplish goals!
> > 
> > BBella: But he said some of the forms are conscious and some are not. If conscious energy is what was from/in the beginning, then how can there be unconscious forms? From what would conscious energy form the unconscious form from?
> 
> I simply think all eternal energy was conscious. I don't think consciousness can appear de novo from nothing. The original energy was conscious.-I get that, but that doesn't answer my question. If eternal conscious energy was first (in the beginning), from what could consciousness make forms that are unconscious?

Genome complexity: mechanism stopped evolving

by David Turell @, Friday, May 13, 2016, 00:25 (2878 days ago) @ BBella


> > David: I simply think all eternal energy was conscious. I don't think consciousness can appear de novo from nothing. The original energy was conscious.
> 
> Bbella: I get that, but that doesn't answer my question. If eternal conscious energy was first (in the beginning), from what could consciousness make forms that are unconscious?-Why couldn't a conscious mind invent simpler forms with no consciousness?

Genome complexity: mechanism stopped evolving

by BBella @, Friday, May 13, 2016, 05:35 (2877 days ago) @ David Turell


> > > David: I simply think all eternal energy was conscious. I don't think consciousness can appear de novo from nothing. The original energy was conscious.
> > 
> > Bbella: I get that, but that doesn't answer my question. If eternal conscious energy was first (in the beginning), from what could consciousness make forms that are unconscious?
> 
> Why couldn't a conscious mind invent simpler forms with no consciousness?-Out of what? Nothing?

Genome complexity: mechanism stopped evolving

by David Turell @, Friday, May 13, 2016, 15:25 (2877 days ago) @ BBella


> > > > David: I simply think all eternal energy was conscious. I don't think consciousness can appear de novo from nothing. The original energy was conscious.
> > > 
> > > Bbella: I get that, but that doesn't answer my question. If eternal conscious energy was first (in the beginning), from what could consciousness make forms that are unconscious?
> > 
> > David: Why couldn't a conscious mind invent simpler forms with no consciousness?
> 
> BBella: Out of what? Nothing?-An existing conscious energy is not nothing. It has always existed in my view and can separate off simpler forms that are not conscious. The universe appears to have been created. It is not conscious, except through us. We have been developed from an inorganic universe, all controlled by the universal mind which manages all development.

Genome complexity: mechanism stopped evolving

by dhw, Thursday, May 12, 2016, 17:58 (2878 days ago) @ BBella

DAVID: And I still think God would not have bothered with all this without keeping an eye on it to be sure it worked out like He intended. All inventors have purposes in mind.
dhw: I had suggested he kept an eye on it because maybe he invented it precisely in order to keep an eye on it - i.e. as the hidden audience, the intention being an enjoyably unpredictable spectacle (see below), though he could always step in. You agree that he's hidden, but you don't like him being an audience - he apparently wants a relationship and that, mysteriously, is why he hides.
DAVID: Spoken like a playwright. What you miss is the obvious requirement of faith, the reason He stays hidden.-Why is faith an “obvious requirement”? Are you now saying that instead of having a “relationship” with humans, he just created them to see whether they would believe in him or not? Since you love asking “why” when we discuss evolution, perhaps you will tell us why God would want to play such a game.
 
BBELLA: In the bible story, God spoke directly to his creation and so no requirement of faith/belief was required from him. -Yes, at least the bible story gives God some sort of motivation: he wants humans to worship him and no other God (“All is vanity” - Ecclesiastes) and to smash up anybody who doesn't believe in him. In fairness, he also wants people to behave nicely to one another and live decently. But that really doesn't require faith in God, does it?-dhw: Or maybe there was just energy in the beginning, and energy kept and keeps transforming itself into all the forms we know and don't know, some of them conscious, some of them not. And that would explain why ATI is such a rich mystery, and why we spend so much time vainly trying to grasp the ungraspable.
DAVID: Your supposition sounds just like conscious energy from the beginning, not requiring much transformation to accomplish goals! 
BBELLA: But he said some of the forms are conscious and some are not.
DAVID: I simply think all eternal energy was conscious. I don't think consciousness can appear de novo from nothing. The original energy was conscious.

Thank you, BBella. My alternative proposal is the reverse of David's: that the beginning was unconscious energy from which eventually, through matter, consciousness emerged, thus leaving a mixture of the conscious and unconscious. But I do not offer it as a belief. I am an agnostic, and have as much difficulty believing consciousness can appear de novo as I do believing that it can simply have always existed without a source.
 
BBELLA: So if the first God, then his angels, then his son werent humans and doesnt sound like an all powerful creator God - what were they? The plot thickens: In walks the alien that fits neatly and perfectly into this scenario. What if I am right? Have you ever asked yourselves that?-Aliens as gods offer us an additional approach but not an alternative solution to the problem of origins. As we have said many times before, in the grand scheme of things the idea only take us one stage further back: how did these superpower aliens come into existence? But that does not mean the hypothesis should not be taken seriously. I think both you and Tony have offered us possible evidence of earlier civilisations, visits from outer space, strange experiences, and there are plenty more examples one can google.…We could even be the descendants of aliens who fled their own planet and settled here. The universe and Earth are so shrouded in mystery, and all proposed solutions are so riddled with uncertainties, that it takes a great deal of faith to choose one and dismiss the rest.

Genome complexity: mechanism stopped evolving

by BBella @, Thursday, May 12, 2016, 22:38 (2878 days ago) @ dhw
edited by BBella, Thursday, May 12, 2016, 22:45

Thank you, BBella. My alternative proposal is the reverse of David's: that the beginning was unconscious energy from which eventually, through matter, consciousness emerged, thus leaving a mixture of the conscious and unconscious. But I do not offer it as a belief. I am an agnostic, and have as much difficulty believing consciousness can appear de novo as I do believing that it can simply have always existed without a source.-Yes, dhw, I understand your take on it, it's Davids I am trying to understand.- 
> BBELLA: So if the first God, then his angels, then his son werent humans and doesnt sound like an all powerful creator God - what were they? The plot thickens: In walks the alien that fits neatly and perfectly into this scenario. What if I am right? Have you ever asked yourselves that?
> 
> Aliens as gods offer us an additional approach but not an alternative solution to the problem of origins. As we have said many times before, in the grand scheme of things the idea only take us one stage further back: how did these superpower aliens come into existence? -I agree. The acknowledgement of the possibility of Aliens (or a much, much older race than our own) does not solve our questions of origin or existence - this is humanities mystery - but may not be theirs. They may know exactly the origin of their and our existence entirely. But give us a few more thousand or hundred years, if not even sooner and we will very likely have the answers as well. ->But that does not mean the hypothesis should not be taken seriously. I think both you and Tony have offered us possible evidence of earlier civilisations, visits from outer space, strange experiences, and there are plenty more examples one can google.…We could even be the descendants of aliens who fled their own planet and settled here. The universe and Earth are so shrouded in mystery, and all proposed solutions are so riddled with uncertainties, that it takes a great deal of faith to choose one and dismiss the rest.-I completely agree! And admit, I do have favorites. But still remaining open for that perfect ONE that embraces all mysteries, leaving none out.

Genome complexity: mechanism stopped evolving

by David Turell @, Friday, May 13, 2016, 00:22 (2878 days ago) @ dhw


> dhw: Why is faith an “obvious requirement”? Are you now saying that instead of having a “relationship” with humans, he just created them to see whether they would believe in him or not? Since you love asking “why” when we discuss evolution, perhaps you will tell us why God would want to play such a game.-We really don't know why He stays concealed. Einhorn's book, A Concealed God, and Schroeder's book, The Hidden Face of God, both discuss it but they don't give firm answers. The leap is required, but I know you won't take it.-> dhw: The universe and Earth are so shrouded in mystery, and all proposed solutions are so riddled with uncertainties, that it takes a great deal of faith to choose one and dismiss the rest.-Exactly!

Genome complexity: mechanism stopped evolving

by dhw, Friday, May 13, 2016, 12:37 (2877 days ago) @ David Turell

dhw: Why is faith an “obvious requirement”? Are you now saying that instead of having a “relationship” with humans, he just created them to see whether they would believe in him or not? Since you love asking “why” when we discuss evolution, perhaps you will tell us why God would want to play such a game.-DAVID: We really don't know why He stays concealed. Einhorn's book, A Concealed God, and Schroeder's book, The Hidden Face of God, both discuss it but they don't give firm answers. The leap is required, but I know you won't take it.-I wonder if they discuss the possibility that the concealment is due to his not actually being there. You still haven't told us why YOU think faith is an “obvious requirement”. Faith in what? That he is there? That's the game I've referred to above. Faith in what else? You always warn us against giving God attributes and intentions (other than producing humans), so it can't be his love, or his plans to give us a bright future after death. A God who is hidden and has no attributes or intentions might just as well not be there, so again, why is faith an “obvious requirement”? Faith in what, and requirement for what?-adhw: The universe and Earth are so shrouded in mystery, and all proposed solutions are so riddled with uncertainties, that it takes a great deal of faith to choose one and dismiss the rest.
DAVID: Exactly!-So faith is required if one is to dismiss all other solutions. Therefore I say unto you and unto Dawkins and unto all who are prepared to listen: “Oh ye of much faith, ye are all leaping in the dark. So acknowledge that you may be wrong and others may be right, and therefore exchange your views with modest humility and with tolerance. Just like us agnostics.”:-)

Genome complexity: mechanism stopped evolving

by David Turell @, Friday, May 13, 2016, 16:08 (2877 days ago) @ dhw

dhw: A God who is hidden and has no attributes or intentions might just as well not be there, so again, why is faith an “obvious requirement”? Faith in what, and requirement for what? - Faith is accepting that God exists and created all of reality. That is obvious. Why are you questioning it? His attributes and intentions are implied and open to human discussion. That is why there are 6,000 religions. - 
> dhw: So faith is required if one is to dismiss all other solutions. - Now you understand! A breakthrough! You of no faith flounder. ;-)

Genome complexity: mechanism stopped evolving

by dhw, Saturday, May 14, 2016, 10:47 (2876 days ago) @ David Turell

Bbella: If eternal conscious energy was first (in the beginning), from what could consciousness make forms that are unconscious?
David: Why couldn't a conscious mind invent simpler forms with no consciousness?

BBella: Out of what? Nothing?
DAVID: An existing conscious energy is not nothing. It has always existed in my view and can separate off simpler forms that are not conscious. -Like BBella, I don't understand how conscious energy can be the only thing in existence and yet separate its own simpler unconscious forms. You now have a God who is part conscious and part unconscious.-DAVID: The universe appears to have been created. It is not conscious, except through us. We have been developed from an inorganic universe, all controlled by the universal mind which manages all development.-So your universal mind is separate from the unconscious inorganic universe, which it created out of nothing but its consciousness. As a panentheist, you believe this conscious mind is within AND without BBella's ALL THAT IS. So God is/is not within/separate from the inorganic universe, and is/is not conscious/unconscious. I find this a bit confusing. Perhaps theistic panpsychism will play some role in your thinking, but I'll leave you to sort out the convolutions!-dhw: A God who is hidden and has no attributes or intentions might just as well not be there, so again, why is faith an “obvious requirement”? Faith in what, and requirement for what?
DAVID: Faith is accepting that God exists and created all of reality. That is obvious. Why are you questioning it? His attributes and intentions are implied and open to human discussion. That is why there are 6,000 religions.-As I suggested earlier, then, God just created us to see if we would believe in him or not. So what was this relationship he wanted with us? And you still haven't explained what this belief in his existence and creativity is an obvious requirement for.-dhw: So faith is required if one is to dismiss all other solutions. 
DAVID: Now you understand! A breakthrough! You of no faith flounder. ;-) -We only flounder when we see theists and atheists kidding themselves that reason, science and common sense are on their side, when we ourselves are painfully aware - as you now acknowledge so triumphantly - that reason, science and common sense are on nobody's side, and to be a theist or an atheist you must rely on irrational, non-scientific, non-commonsensical faith. Well, this acknowledgement is indeed a breakthrough! :-D

Genome complexity: mechanism stopped evolving

by David Turell @, Saturday, May 14, 2016, 14:13 (2876 days ago) @ dhw


> dhw: Like BBella, I don't understand how conscious energy can be the only thing in existence and yet separate its own simpler unconscious forms. You now have a God who is part conscious and part unconscious.-If God invented the universe, and I'm sure He did, it is not conscious. If God invented life, and I'm sure He did, He started with bacteria, and they are not conscious.
> 
> DAVID: The universe appears to have been created. It is not conscious, except through us. We have been developed from an inorganic universe, all controlled by the universal mind which manages all development.
> 
> dhw: So your universal mind is separate from the unconscious inorganic universe, which it created out of nothing but its consciousness. As a panentheist, you believe this conscious mind is within AND without BBella's ALL THAT IS. So God is/is not within/separate from the inorganic universe, and is/is not conscious/unconscious. I find this a bit confusing. Perhaps theistic panpsychism will play some role in your thinking, but I'll leave you to sort out the convolutions!-Your problem, not mine. The inorganic universe with its lately arrived living portion has a universal consciousness, God.
> 
> dhw: So faith is required if one is to dismiss all other solutions. -> DAVID: Now you understand! A breakthrough! You of no faith flounder. ;-) 
> 
> dhw: We only flounder when we see theists and atheists kidding themselves that reason, science and common sense are on their side, when we ourselves are painfully aware - as you now acknowledge so triumphantly - that reason, science and common sense are on nobody's side, and to be a theist or an atheist you must rely on irrational, non-scientific, non-commonsensical faith. Well, this acknowledgement is indeed a breakthrough! :-D-Funny, but I started as an agnostic, looked at the science and found faith. My mind does not work like yours. Not surprising, we all have our own approaches and prejudices.

Genome complexity: mechanism stopped evolving

by dhw, Sunday, May 15, 2016, 17:52 (2875 days ago) @ David Turell

dhw: Like BBella, I don't understand how conscious energy can be the only thing in existence and yet separate its own simpler unconscious forms. You now have a God who is part conscious and part unconscious.-DAVID: If God invented the universe, and I'm sure He did, it is not conscious. If God invented life, and I'm sure He did, He started with bacteria, and they are not conscious.-But if nothing existed except consciousness, what did consciousness make an unconscious universe from? As regards bacteria, their non-consciousness is a matter of opinion not fact.-DAVID: The universe appears to have been created. It is not conscious, except through us. We have been developed from an inorganic universe, all controlled by the universal mind which manages all development.
dhw: So your universal mind is separate from the unconscious inorganic universe, which it created out of nothing but its consciousness. As a panentheist, you believe this conscious mind is within AND without BBella's ALL THAT IS. So God is/is not within/separate from the inorganic universe, and is/is not conscious/unconscious. I find this a bit confusing. Perhaps theistic panpsychism will play some role in your thinking, but I'll leave you to sort out the convolutions!
DAVID: Your problem, not mine. The inorganic universe with its lately arrived living portion has a universal consciousness, God.-Ah well, I guess that's one way of ending a discussion. 
 
dhw: So faith is required if one is to dismiss all other solutions. 
DAVID: Now you understand! A breakthrough! You of no faith flounder. ;-) 
dhw: We only flounder when we see theists and atheists kidding themselves that reason, science and common sense are on their side, when we ourselves are painfully aware - as you now acknowledge so triumphantly - that reason, science and common sense are on nobody's side, and to be a theist or an atheist you must rely on irrational, non-scientific, non-commonsensical faith. Well, this acknowledgement is indeed a breakthrough! :-D 
DAVID: Funny, but I started as an agnostic, looked at the science and found faith. My mind does not work like yours. Not surprising, we all have our own approaches and prejudices.-Very true. If all our minds worked alike, there would be nothing to discuss!

Genome complexity: mechanism stopped evolving

by David Turell @, Sunday, May 15, 2016, 20:22 (2875 days ago) @ dhw


> DAVID: If God invented the universe, and I'm sure He did, it is not conscious. If God invented life, and I'm sure He did, He started with bacteria, and they are not conscious.
> 
> dhw: But if nothing existed except consciousness, what did consciousness make an unconscious universe from? As regards bacteria, their non-consciousness is a matter of opinion not fact.-What is your definition of consciousness? All Shapiro appears to allude to is a possibility of minor conscious reactions, not introspection. Next, energy and matter are interchangeable. God's conscious energy just transformed some of itself into the matter of the universe, and remember, as a panentheist, I view His consciousness is within and without the universe.
> 
> DAVID: The universe appears to have been created. It is not conscious, except through us. We have been developed from an inorganic universe, all controlled by the universal mind which manages all development.-> dhw: So your universal mind is separate from the unconscious inorganic universe, which it created out of nothing but its consciousness. As a panentheist, you believe this conscious mind is within AND without BBella's ALL THAT IS. So God is/is not within/separate from the inorganic universe, and is/is not conscious/unconscious. I find this a bit confusing. Perhaps theistic panpsychism will play some role in your thinking, but I'll leave you to sort out the convolutions!-> DAVID: Your problem, not mine. The inorganic universe with its lately arrived living portion has a universal consciousness, God.
> 
> dhw: Ah well, I guess that's one way of ending a discussion.-I'm sorry.In my earlier statement I assumed what you stated above. You have simply fleshed out my thinking more clearly. To review, God is a consciousness within and without the universe, but the early inorganic universe was not in and of itself conscious until conscious living forms appeared. Consciousness at the level of ours, somewhat mimicking God's, finally appeared late.
>

Genome complexity: mechanism stopped evolving

by dhw, Monday, May 16, 2016, 16:09 (2874 days ago) @ David Turell

DAVID: If God invented the universe, and I'm sure He did, it is not conscious. If God invented life, and I'm sure He did, He started with bacteria, and they are not conscious.
dhw: But if nothing existed except consciousness, what did consciousness make an unconscious universe from? As regards bacteria, their non-consciousness is a matter of opinion not fact.-DAVID: What is your definition of consciousness? All Shapiro appears to allude to is a possibility of minor conscious reactions, not introspection.-So far as I know, nobody has ever suggested that bacteria are introspective, or that their intelligence/consciousness is to be equated with human consciousness. Once more: the term denotes such attributes as sentience, the ability to register and process information, to communicate and cooperate, to take decisions and solve problems.-DAVID: Next, energy and matter are interchangeable. God's conscious energy just transformed some of itself into the matter of the universe. -The “interchangeability” of energy and matter presents a problem here. It fits in with the hypothesis that first cause is an unconscious process of energy and matter eternally transmuting themselves into each other, with matter somehow - the great improbability - becoming aware of the changes. (Awareness is meaningless unless there is something to be aware of.) However, your first cause is nothing but eternal conscious energy which at some finite time in the past deliberately transformed "some of itself" into unconscious matter. They are not “interchangeable” in your scenario, because the one is conscious and actually creates the other, which is unconscious. -DAVID: […] To review, God is a consciousness within and without the universe, but the early inorganic universe was not in and of itself conscious until conscious living forms appeared. Consciousness at the level of ours, somewhat mimicking God's, finally appeared late.-I think theistic panpsychists would say that the inorganic universe contains particles of their God, and so are “quasi-conscious” (Oxford Companion to Philosophy). In an atheistic version, this quasi-consciousness would have come about as described above. As an agnostic, I thoroughly approve of your neutral “conscious living forms appeared”. As a fan of the “cellular intelligence” hypothesis, I also approve of these early living forms being described as “conscious”, though not the same as “consciousness at the level of ours”. Thank you. That is precisely the concept which I have been trying to explain for the last few years and which you have so resolutely opposed! :-)

Genome complexity: mechanism stopped evolving

by David Turell @, Monday, May 16, 2016, 17:59 (2874 days ago) @ dhw


> dhw: So far as I know, nobody has ever suggested that bacteria are introspective, or that their intelligence/consciousness is to be equated with human consciousness.-Agreed at that level.-> dhw> Once more: the term denotes such attributes as sentience, the ability to register and process information, to communicate and cooperate, to take decisions and solve problems.-All of which can be explained as automatic in molecular reactions and feedback loops.
> 
> DAVID: Next, energy and matter are interchangeable. God's conscious energy just transformed some of itself into the matter of the universe. 
> 
> dhw: The “interchangeability” of energy and matter presents a problem here. It fits in with the hypothesis that first cause is an unconscious process of energy and matter eternally transmuting themselves into each other, with matter somehow - the great improbability - becoming aware of the changes. (Awareness is meaningless unless there is something to be aware of.)-Disagree. God as pure energy can be aware of Himself. Why He cannot create matter (which will be unconscious) is not reasonable. Of course, if God has all the attributes assigned to Him, He can create matter from some of His energy.-> dhw: However, your first cause is nothing but eternal conscious energy which at some finite time in the past deliberately transformed "some of itself" into unconscious matter. They are not “interchangeable” in your scenario, because the one is conscious and actually creates the other, which is unconscious.-All particle which form matter are points of energy. E=mC^2. Interchangeable. Pure unconscious matter is potential energy. It is separated in our universe, and if God made this universe, the separation occurred.
> 
> dhw: As an agnostic, I thoroughly approve of your neutral “conscious living forms appeared”. As a fan of the “cellular intelligence” hypothesis, I also approve of these early living forms being described as “conscious”, though not the same as “consciousness at the level of ours”.-In that statement I am referring to multicellular early forms with a brain, as in the Cambrian Explosion. They were obviously conscious and aware of their surroundings. Don't try to extrapolate my thinking back beyond that. I've made the exact point before.

Genome complexity: mechanism stopped evolving

by BBella @, Tuesday, May 17, 2016, 00:12 (2874 days ago) @ David Turell

DAVID: Next, energy and matter are interchangeable. God's conscious energy just transformed some of itself into the matter of the universe. 
> > 
> > dhw: The “interchangeability” of energy and matter presents a problem here. It fits in with the hypothesis that first cause is an unconscious process of energy and matter eternally transmuting themselves into each other, with matter somehow - the great improbability - becoming aware of the changes. (Awareness is meaningless unless there is something to be aware of.)
> 
>[david] Disagree. God as pure energy can be aware of Himself. Why He cannot create matter (which will be unconscious) is not reasonable. Of course, if God has all the attributes assigned to Him, He can create matter from some of His energy.-If there were such a thing as a beginning (and I doubt that), and in that beginning was ONLY conscious mind (God), then every thing made was/is created from that very fabric of that first conscious mind (God). Which would mean, All that now IS, is made up of the fabric of that conscious mind (God). It is illogical and VERY difficult to believe that consciousness can be taken out of itself to create the unconscious. And the bigger question, even if possible, would be why? Instead of making creation into the unconscious dead, why not make it into (or even better - become) an ongoing, ever changing event that never ceases to be - which is what consciousness is? -So, if in fact, it were true, that in the beginning, conscious mind was alone and all that was, then this would also have to be true and makes more sense to me; paraphrasing Rumi: consciousness now sleeps in the rocks, awakens in the fish and dances in man. -In other words: All that IS, vibrates at differing quantum speeds, creating all that we see and don't see, and IS all that IS.

Genome complexity: mechanism stopped evolving

by David Turell @, Tuesday, May 17, 2016, 01:28 (2874 days ago) @ BBella


> Bbella: If there were such a thing as a beginning (and I doubt that), and in that beginning was ONLY conscious mind (God), then every thing made was/is created from that very fabric of that first conscious mind (God). Which would mean, All that now IS, is made up of the fabric of that conscious mind (God). -As I've reminded dhw, energy and matter are one and the same interchangeable states. E=mC^2 I see no reason why God could not convert some energy to matter as our universe. God's mind is eternal energy. I agree.-> Bbella: And the bigger question, even if possible, would be why? Instead of making creation into the unconscious dead, why not make it into (or even better - become) an ongoing, ever changing event that never ceases to be - which is what consciousness is? -We agree consciousness is at the basis of quantum mechanics and the universe
> 
> > Bbella: So, if in fact, it were true, that in the beginning, conscious mind was alone and all that was, then this would also have to be true and makes more sense to me; paraphrasing Rumi: consciousness now sleeps in the rocks, awakens in the fish and dances in man. -Agreed.
> 
> Bbella: In other words: All that IS, vibrates at differing quantum speeds, creating all that we see and don't see, and IS all that IS.-For me that is God working always through quantum mechanics.

Genome complexity: mechanism stopped evolving

by dhw, Tuesday, May 17, 2016, 11:57 (2873 days ago) @ David Turell

dhw: Once more: the term denotes such attributes as sentience, the ability to register and process information, to communicate and cooperate, to take decisions and solve problems.
DAVID: All of which can be explained as automatic in molecular reactions and feedback loops.-You asked me to define non-human consciousness. Under “algae” you told us that early living forms with brains were conscious. You seem to agree that the above attributes are present in bacteria, but say they are “automatic”, so may I please ask you in turn to explain what additional attributes are possessed by conscious organisms with brains, apart from humans.-DAVID: Next, energy and matter are interchangeable. God's conscious energy just transformed some of itself into the matter of the universe. 
dhw: The “interchangeability” of energy and matter presents a problem here […] 
DAVID: Disagree. God as pure energy can be aware of Himself. Why He cannot create matter (which will be unconscious) is not reasonable. Of course, if God has all the attributes assigned to Him, He can create matter from some of His energy.-If you say God can do anything, he can do anything. End of discussion. But let's go on. My problem here is with what you have called interchangeability. If consciousness can turn itself into unconsciousness, can unconsciousness turn itself into consciousness? Can the planet Jupiter turn itself into the god Jupiter? Seems unlikely. The problem BBella*** and I have raised is that if nothing, absolutely nothing existed except conscious energy (there was no matter), how could it suddenly make itself into separate, unconscious matter? They are clearly NOT interchangeable. Whereas an endless first cause process of energy and matter being transformed into one another gets rid of that problem (though it doesn't solve the problem of how consciousness arose).
***This was written before I had seen BBella's latest post and your reply, which again emphasizes interchangeability.-DAVID: All particles which form matter are points of energy. E=mC^2. Interchangeable. Pure unconscious matter is potential energy. It is separated in our universe, and if God made this universe, the separation occurred.-I have no problem with matter as potential energy. I do have problems with unconscious matter springing from conscious energy, and the two being separate but interchangeable.-dhw: As an agnostic, I thoroughly approve of your neutral “conscious living forms appeared”. As a fan of the “cellular intelligence” hypothesis, I also approve of these early living forms being described as “conscious”, though not the same as “consciousness at the level of ours”.
DAVID: In that statement I am referring to multicellular early forms with a brain, as in the Cambrian Explosion.
 
My apologies. When you said the early inorganic universe was not conscious until conscious living forms appeared, I assumed you were referring to early life, not forms that did not appear until some 3 billion years later. You see, I live in hope!

Genome complexity: mechanism stopped evolving

by BBella @, Wednesday, May 11, 2016, 19:59 (2879 days ago) @ dhw

God would not be your common inventor as we know inventors to be. It seems to me, if there were an all wise God, who in the beginning created all that IS and then rested from his works and let be, as the scriptures testify, I would think that kind of God would have no need to fiddle, as he would have already implanted every need, variation and ability needed into All That IS. Not to say, as the scriptures also testify, he didn't fiddle with the plans of man.[/i]-I meant to say, "as the scriptures also testify, he did fiddle with the plans of man".
> 
>[dhw] Maybe he's not all wise. Maybe he's a process God, learning as he goes. Wouldn't it be incredibly boring to know everything? Do you enjoy novels, plays, films whose plot developments and denouement are already obvious from the start?-I agree, if he's a process God, learning as he goes, this would be so. The premise above was: If he were an all wise God that rested, as the scriptures posit. 
> 
> BBELLA: But as you know, if there was A God in the beginning, what I think is more likely the case, God multiplied and became ALL That IS which explains why ATI is so brilliant! And that simply explains everything except how.
> 
> Or maybe there was just energy in the beginning, and energy kept and keeps transforming itself into all the forms we know and don't know, some of them conscious, some of them not. And that would explain why ATI is such a rich mystery, and why we spend so much time vainly trying to grasp the ungraspable.-In my above statement, I was going on Davids premise, "if there was a God in the beginning before ATI (not the scriptural beginning). But I agree more with your above statement and believe it more likely to be the case. But as you know, the way I see the scenario more likely unfolded was: If there were a beginning, energy came first - then formed beings we dont know, that we now call God/gods, that probably created beings we do know, humans. Round and round we go...

Genome complexity: epigenetics in diagrams

by David Turell @, Saturday, May 14, 2016, 05:58 (2876 days ago) @ BBella

I cannot give excerpts. look at the illustrations and the commentary: - http://blogs.scientificamerican.com/sa-visual/gene-regulation-illustrated/?WT.mc_id=SA_... - Just a sense of the complexity

Genome complexity: plants control gene expression

by David Turell @, Sunday, May 22, 2016, 15:17 (2868 days ago) @ David Turell

Researchers have mapped out regions of non-coding DNA that control gene expression and transcription in plants, another example of 'junk DNA goodbye!':-https://www.sciencedaily.com/releases/2016/05/160519130231.htm-"New findings yield insights into how plants get their traits. Revealing a landscape of protein-binding zones on DNA, collectively dubbed the "cistrome," shows how plants control where and when genes are expressed.-***-"Revealing this landscape of protein-binding zones on DNA, collectively dubbed the "cistrome," shows how plants control where and when genes are expressed. Previous methods for mapping the cistrome in plant cells were difficult and slow, but the new approach, detailed in the May 19, 2016 issue of Cell, overcomes those hurdles to offer a sweeping view of this critical aspect of genetic regulation.-"This is one of the first efforts to globally characterize all the regulatory elements in a plant genome," says senior author Joseph Ecker, professor and director of Salk's Genomic Analysis Laboratory and holder of the Salk International Council Chair in Genetics. "The cistrome has been a missing piece of information for trying to understand how plants function."-***-"To test out the utility of DAP-seq, Ecker, Huang, O'Malley and their colleagues mapped where 529 transcription factors bound to the genome of Arabidopsis thaliana, the plant most studied by scientists. They identified 2.7 million binding sites. They then repeated the experiments using DNA containing or not containing cytosine methylation--a process of marking the genome's surface with chemical methyl tags to further inhibit or activate genes. The binding patterns of about three-quarters of the transcription factors that they tested changed.-"'This allowed us to expose binding sites that we might miss if we didn't remove the methylation. With this approach we can see binding sites that may be active in only a subset of cells or tissues," says O'Malley. The new results show not only how regulatory proteins alter gene expression, but the roles the epigenomic methylation marks may play in this regulation.-***-"Ecker and collaborating groups at Duke University and the University of Western Australia revealed that different types of cells in the Arabidopsis root have different patterns of methylation. Using DAP-seq, they'll now be able to study how those patterns in root cells affect the binding of transcription factors."-Comment: Just another example of the fact that much of the DNA in plants and animals is useful, not junk. DNA is manufacturing proteins for replacement, but it must regulate speed of production, where the proteins go, how the various organ systems are coordinated and regulated, among many obvious duties beyond coding for protein. It is amazing this was not obvious to science years ago, but Darwin dedicated scientists used the concept of 'junk DNA' in a twisted way to support Darwin theory of chance evolution: if it didn't code, it was junk, left over from previous attempts to advance by chance mutations.

Genome complexity: horizontal gene transfer

by David Turell @, Saturday, June 04, 2016, 14:52 (2855 days ago) @ David Turell

HGT is well recognized between bacteria conveying antibiotic resistance , but is now discovered from microbiome to insect animals. Doesn't make new species but allows for adaptations:-https://www.sciencedaily.com/releases/2016/05/160531112717.htm-"Many plant-feeding insects need microbial enzymes, such as pectinases, that degrade plant cell walls; yet some insects have overcome this dependency in a surprising way. Now researchers found that stick insects make microbial enzymes themselves. From an ancestral gut microbe, the genes for the essential enzymes simply 'jumped' as they are to their insect host. -"Many animals depend on their microbiome to digest their food. Symbiotic microorganisms produce enzymes their hosts cannot, and these work alone or together with the animals' own enzymes to break down their food. Many plant-feeding insects need microbial enzymes, such as pectinases, that degrade plant cell walls; yet some insects have overcome this dependency in a surprising way. Researchers at the Max Planck Institute for Chemical Ecology in Jena, Germany, found that stick insects make microbial enzymes themselves. From an ancestral gut microbe, the genes for the essential enzymes simply "jumped" as they are to their insect host. The researchers report this newly discovered "horizontal gene transfer" in a paper recently published in Scientific Reports.-"Insects are not supposed to make their own pectinases," explains Dr. Matan Shelomi, a postdoctoral fellow in the Department of Entomology and lead author of the study. Yet the stick insects make lots, and their genome contains multiple pectinase genes!" Based on DNA similarity, the source was a gamma-proteobactera, the most common bacteria type in the stick insect microbiome, but commonly found on the leaves they eat too. "We are not sure how it happened, but one or two pectinase genes from a gut bacterium or even just something in the food clearly jumped into the stick insect genome, and then evolved along with the insects," explains Shelomi. Tests show some of the new pectinases retained their original job degrading pectin, while others have yet unknown functions. But when did the transfer happen?-***-"The results showed that the gene jump occurred sometime after Timema and Euphasmatodea split, but before the latter diverged into the 3000 or so species it has today: between 110 to 60 million years ago.-***-"Something happened, to make the tiny Timema become a planet-wide group of nearly 3000 species that can be nearly half a meter long," says Shelomi, referring to the world's longest insect, a Euphasmatodea called Phoebetica chani. His new theory, the Enzyme Expansion Hypothesis, is that the sudden appearance of new enzyme abilities, either through mutation or horizontal gene transfer, can drive the evolution of a species and change their diets to specialize on a single food source.-"Beyond enzymes, horizontal gene transfer can provide any number of new abilities, and our microbiome provides an immense source of potential species-altering proteins. "The idea that genes from microbes living in our guts can suddenly become part of our genomes and change the course of our evolutionary history, that's an incredible finding," Shelomi concludes."-Comment: Another 'not Darwin' type of evolutionary change. It modifies the abilities of a species but does not make a new one.

Genome complexity: horizontal gene transfer

by David Turell @, Monday, June 13, 2016, 15:30 (2846 days ago) @ David Turell

New computer simulation research on cell division mechanics may have found the way that human cells organize 46 chromosomes into 23 pairs from six feet of DNA when packed into a nucleus. The nucleus opens and the pairs are split, all in a 20 minute space of time as the cell divides in two:-http://phys.org/news/2016-06-chromosomes-tiny-loops-molecular-motors.html-
"Human cells contain 23 pairs of chromosomes that form a loosely organized cluster in the cell nucleus. When cells divide, they must first condense these chromosomes—each of which when fully extended is a thousand times longer than the cell's nucleus and physically indistinguishable from the others—into compact structures that can be easily separated and packaged into their offspring. -"An MIT-led team has now developed a model that explains how cells handle this difficult task. In computer simulations, the researchers demonstrate that certain molecular "machines" can transform chromosomes from a loosely tangled rope into a series of tiny loops that condense each chromosome and allow it to extricate itself from the others.-"Moreover, the researchers demonstrate that a similar model explains how chromosomes are organized when cells are not dividing, and they hypothesize that loop extrusion by molecular motors splits chromosomes into separate domains, helping to control which genes are expressed in a given cell.-"This mechanism, outlined in three recent papers published in Cell Reports, eLife, and Biophysical Journal, suggests that chromosome organization relies on proteins that act as molecular motors that pull strands of DNA into progressively larger loops. The MIT team suggests that two proteins thought to function primarily as "staples" that hold DNA together, cohesin and condensin, can also actively manipulate DNA.-"'Nobody has ever directly observed this mechanism of loop extrusion. If it exists, it will solve lots of problems," says Leonid Mirny, a professor of physics in MIT's Institute for Medical Engineering and Sciences, who led the research. "We will know how chromosomes condense, how they segregate, how genes talk to enhancers. Lots of things can be solved by this mechanism."-"'What we believe is happening is each condensin complex consists of two motors, each moving along the chromosome in the opposite direction," Mirny says. "Each loop extrusion event is tiny compared to the size of a chromosome. Nevertheless, collectively they can self-organize this chromosome into an early-metaphase, condensed chromosome."-"In human cells, this process usually takes about 20 minutes.-"The loops seen during interphase are constantly being formed and then dismantled in a dynamic process. When a cell begins preparing to divide, the researchers believe the boundaries are removed and condensin comes in to form the many more loops needed to condense the chromosomes for cell division.-"Although biologists have not demonstrated that condensin and cohesin can act as molecular motors, there is speculation that they can because they are structurally similar to other cellular proteins that function as molecular motors.-"'Combined, these papers constitute the most important papers in our field in the last five years," says Job Dekker, a professor of biochemistry and molecular pharmacology at the University of Massachusetts Medical School, who was not involved in the research. "These papers explain how a very simple method of loop extrusion can explain, to an extraordinary level, the structures of chromosomes in both mitotic and nondividing cells.'"-Comment: Cell division is a constant activity in life. The DNA in its chromosome form must be split accurately every time. Obviously there are mistakes, but controls reduce them to a very bare minimum. Look at this website to see how complex the many phases are:- https://askabiologist.asu.edu/content/cell-division-Not by chance!

Genome complexity: variation within species

by David Turell @, Friday, December 09, 2016, 15:28 (2667 days ago) @ David Turell

It turns out checking one individual's genome in a species is not the whole story. To understand a species variability many individuals have to be sequenced. This is one species that can adapt to almost anything:

http://phys.org/news/2016-12-evolution-action-fish-quickly-lethal.html

"The killifish is up to 8,000 times more resistant to this level of pollution than other fish, the study found. While the fish is not commercially valuable, it is an important food for other species and an environmental indicator.

"What makes Atlantic killifish so special? Extremely high levels of genetic variation, higher than any other vertebrate—humans included—measured so far. The more genetic diversity, the faster evolution can act. That's one reason why insects and weeds can quickly adapt and evolve to resist pesticides, and why pathogens can evolve quickly to resist drugs created to destroy them.

"Some people will see this as a positive and think, 'Hey, species can evolve in response to what we're doing to the environment!'" said lead author Andrew Whitehead, associate professor in the UC Davis Department of Environmental Toxicology. "Unfortunately, most species we care about preserving probably can't adapt to these rapid changes because they don't have the high levels of genetic variation that allow them to evolve quickly."

"The scientists sequenced complete genomes of nearly 400 Atlantic killifish from polluted and nonpolluted sites at New Bedford Harbor in Massachusetts; Newark Bay, New Jersey; Connecticut's Bridgeport area; and Virginia's Elizabeth River. The sites have been polluted since the 1950s and 1960s by a complex mixture of industrial pollutants including dioxins, heavy metals, hydrocarbons and other chemicals.

"The team's genetic analysis suggests that the Atlantic killifish's genetic diversity make them unusually well positioned to adapt to survive in radically altered habitats. At the genetic level, the tolerant populations evolved in highly similar ways. This suggests that these fish already carried the genetic variation that allowed them to adapt before the sites were polluted, and that there may be only a few evolutionary solutions to pollution.

***

"This study shows that different populations of Atlantic killifish exposed to toxic pollution evolve tolerance to that pollution through changes in one molecular pathway," said George Gilchrist, program director in the National Science Foundation's Division of Environmental Biology, which funded the study along with the National Institute of Environmental Health Sciences. "This pathway may play a similar role in many animals exposed to pollutants, with slightly different adaptations in response to different toxicants.'"

Comment: It is becoming recognized that alternate metabolic pathways may be present in many species, as I noted in our previous discussions about bacteria responding to antibiotics (can't find the reference). The species is still one species. It is not a new evolutionary process as the articles headline proclaims. I have another article on tis subject to present later today.

Genome complexity: variation within species

by David Turell @, Friday, December 09, 2016, 18:51 (2667 days ago) @ David Turell

We had a discussion over an article BBella presented about E. coli learning to fight with antibiotics. I made the point that bacteria have alternative pathways, have variability within a species and can overcome the antibiotic if given time to make the adaptations or allow the résistance members of the species to survive and reproduce, and it was not new evolution but a use of available alternatives. This was her reference (Wednesday, October 05, 2016, 15:59) :

https://www.wired.com/2016/09/gorgeous-unsettling-video-evolution-action/

Now the scientific community is recognizing this genomic variability which comes in evolved organisms:

http://www.the-scientist.com/?articles.view/articleNo/47510/title/The-Pangenome--Are-Si...

"with genome sequencing becoming faster, cheaper, and more accessible all the time, it quickly became apparent that this attitude overlooked one very important aspect of biology—genomic variation among individuals. And for some species, such variation can be significant. In the early 2000s, for example, when Tettelin, then at the Institute for Genomic Research (TIGR), and his colleagues compared eight isolates of Streptococcus agalactiae (or group B Streptococcus, GBS), they found not only the small, within-gene variations predicted by conventional genetics, but an average of 33 completely new genes with every new genome sequenced. “It was a shock,” says Tettelin. “We saw there were many regions—relatively large regions—of diversity.”

***

"Over the past 10 years, large-scale sequencing projects have revealed startling levels of individual genomic variation across the tree of life, challenging the value of the modern reference genome—as well as the very notion of a species. To better capture the genetic makeup of any given taxon, many researchers now argue that the field of genomics should adopt a pangenomic framework in which diversity is central, rather than incidental, to our view of species.

***

"The pangenome concept has since been widely adopted by research groups trying to keep track of newly discovered diversity within and among bacterial taxa. In addition to high recombination rates and mobile genetic elements, which have long been known to be drivers of prokaryotic diversity, horizontal gene transfer—direct or indirect exchange of genetic material among even unrelated organisms—is proving to contribute to individual diversity across the bacterial domain and beyond.

"Bacteria have “access to a toolkit within species and across species,” Tettelin explains. For taxa with large, open pangenomes—often a reflection of high rates of gene transfer—that toolkit corresponds to a theoretically unlimited pool of easy-to-access new biological functions. “They’re essentially champions at versatility and adaptability,” he says.

***

"To date, researchers have applied the pangenome framework to some 50 bacterial species, including model organisms, such as E. coli, and commercially significant microbes, such as the wine bacterium Oenococcus oeni. Scientists have used the same basic principles to consider shared and variable genes and gene families within larger groups such as genera, the human microbiome, and even the entire bacterial domain. Now, with the approach broadly accepted as a useful way to organize bacterial diversity, efforts are focusing on incorporating this more variation-centric view into metagenomics, phylogenetics, and even taxonomy itself.

“'We have learned a tremendous amount about the machinery of life from model organisms that have been studied in the lab, but we haven’t really confronted head-on the role of the diversity,” says Chisholm. “Now I think we’re learning that this diversity is part of what life is all about.”

***

"Although variation in genomic content between two humans is minuscule in comparison with that of microbes or plants, the earliest attempt at building a human pangenome in 2009—based on the human reference genome and just two others—estimated that up to 40 megabases of sequence, including protein-coding regions, were absent from the reference genome. (my bold)

***

"Even in the eukaryotic world, where genomic fluidity is far less pronounced, pangenomic analyses have cast new light on conventional taxonomies. Sequencing of multiple individuals in several groups of eukaryotic organisms, from marine phytoplankton to crop plants, have challenged traditional notions of within-species diversity and raised the question of what “species” even means. If the goal of classification is to create biologically useful groups of like organisms, then such questions are important to resolve—yet for now, at least, they’re still very much open."

Comment: Variability within species obviously common. That humans are not so variable supports my idea that we are the end of the evolution process. We have so much control of our lives we don't need the variability.

Genome complexity: variation within species

by dhw, Saturday, December 10, 2016, 12:15 (2666 days ago) @ David Turell

Thank you for these three posts, which I am combining since they all relate to the same subject.

DAVID (under "genome complexity”): Cells are constantly reproducing themselves as daughters. DNA must be constantly monitored against mistakes, and it is:
http://www.businessinsider.com/breakthrough-prize-winner-dna-research-2016-12

SELECTED QUOTES (my bold):
"That DNA tells our cells what to do. When they divide, that information is copied from one cell to another."

"It's only thanks to a mechanism in our cells that can recognize when something has gone wrong that we aren't all riddled with cancer."

"That mechanism, known as the DNA damage response, functions like an individual intelligent agent, able to monitor when things are going wrong and then try to come up with a way to deal with them."

"'One of the remarkable properties of nature’s most remarkable molecule, DNA, is self-awareness: it can detect information about its own integrity and transmit that information back to itself,"

"When this response detects damaged DNA, it can respond in several ways.”

David’s comment: There is no way life could have continued with a DNA code controlling it, unless such a defense mechanism against mistakes was present at all times. Only a saltation could have produced this result. Not by chance.

As always, a powerful case for design. But design of what? A microcosm within a macrocosm? “DNA tells our cells what to do…a mechanism that can recognize…like an individual intelligent agent…try to come up with a way…self-awareness…respond in several ways…” So many of the actions and attributes we associate with intelligence – and yet we are not even aware of them. It’s as if we are inhabited by a colony of ants, each with their own particular role to play, but constantly communicating, adapting, making decisions in the world that is you or me. It’s what some scientists call cellular intelligence.
xxxxxxx
QUOTE (re the killifish): "The team's genetic analysis suggests that the Atlantic killifish's genetic diversity make them unusually well positioned to adapt to survive in radically altered habitats. At the genetic level, the tolerant populations evolved in highly similar ways. This suggests that these fish already carried the genetic variation that allowed them to adapt before the sites were polluted, and that there may be only a few evolutionary solutions to pollution.

David’s comment: It is becoming recognized that alternate metabolic pathways may be present in many species, as I noted in our previous discussions about bacteria responding to antibiotics (can't find the reference). The species is still one species. It is not a new evolutionary process as the articles headline proclaim.

May I suggest that if the killifish is able to cope so quickly with different pollutants, what it carries before the sites are polluted is not an alternative metabolic pathway anticipating whatever might happen next, but the ability to process new information and change its genome accordingly – which means it can construct a new metabolic pathway to cope with each new threat. And I would suggest that this applies to all processes of adaptation, though different organisms will have different capacities for change. You are quite right: this is not the same as innovation. It is simply confirmation that the genome can be changed when an organism experiences new conditions. We don’t know how far the ability for change can extend. Or do you still think your God put each alternative metabolic pathway for all eventualities into the first cells to pass on to the killifish a few thousand million years later?
xxxxxxx
QUOTE: "Over the past 10 years, large-scale sequencing projects have revealed startling levels of individual genomic variation across the tree of life, challenging the value of the modern reference genome—as well as the very notion of a species. To better capture the genetic makeup of any given taxon, many researchers now argue that the field of genomics should adopt a pangenomic framework in which diversity is central, rather than incidental, to our view of species.”

Nobody has yet solved the problem of defining species (Darwin devotes a whole section to it), which is why I usually put “broad sense” in parentheses, since it is the borderlines that are blurred. Nobody would claim they can’t distinguish between, say, elephant species and butterfly species. But what is really interesting is the variability between individuals. This would explain how common descent works. Changes can only take place in individuals, and individuals are different. So some will respond to environmental change and others won’t. So far we only know of adaptation and non-adaptation (those that can’t respond will die). But it is conceivable that the variation will also apply to innovation. Some organisms may have the wherewithal to invent. In much the same way as some humans are creative, and some are not.

Genome complexity: variation within species

by David Turell @, Saturday, December 10, 2016, 22:13 (2666 days ago) @ dhw

dhw: As always, a powerful case for design. But design of what? A microcosm within a macrocosm? “DNA tells our cells what to do…a mechanism that can recognize…like an individual intelligent agent…try to come up with a way…self-awareness…respond in several ways…” So many of the actions and attributes we associate with intelligence – and yet we are not even aware of them. It’s as if we are inhabited by a colony of ants, each with their own particular role to play, but constantly communicating, adapting, making decisions in the world that is you or me. It’s what some scientists call cellular intelligence.

The design comes from the intelligent information in DNA. The entire design of the organism. The source of that information is what you and I debate.

xxxxxxx

David’s comment: It is becoming recognized that alternate metabolic pathways may be present in many species, as I noted in our previous discussions about bacteria responding to antibiotics (can't find the reference). The species is still one species. It is not a new evolutionary process as the articles headline proclaim.

dhw: May I suggest that if the killifish is able to cope so quickly with different pollutants, what it carries before the sites are polluted is not an alternative metabolic pathway anticipating whatever might happen next, but the ability to process new information and change its genome accordingly – which means it can construct a new metabolic pathway to cope with each new threat.

On the other hand the article clearly suggests there are variable individuals in the species some of whom can handle the pollution and survive. If the fish are living in pollution they might not survive long enough to produce enough generations of offspring with the ability to survive. You are stretching your theory about cellular abilities to adapt on their own at high speed. I'll repeat current scientific thought as in bacteria. Species variation allows some individuals to survive and adapt the species to a new challenge.

dhw: And I would suggest that this applies to all processes of adaptation, though different organisms will have different capacities for change. You are quite right: this is not the same as innovation. It is simply confirmation that the genome can be changed when an organism experiences new conditions.

This is certainly true if new conditions are not severe and allow for several generations of change.

dhw:We don’t know how far the ability for change can extend. Or do you still think your God put each alternative metabolic pathway for all eventualities into the first cells to pass on to the killifish a few thousand million years later?

Many species have variable individuals who can survive changes, nothing more.

xxxxxxx

dhw: Nobody has yet solved the problem of defining species ... But what is really interesting is the variability between individuals. This would explain how common descent works. Changes can only take place in individuals, and individuals are different. So some will respond to environmental change and others won’t. So far we only know of adaptation and non-adaptation (those that can’t respond will die). But it is conceivable that the variation will also apply to innovation. Some organisms may have the wherewithal to invent. In much the same way as some humans are creative, and some are not.

All organisms can adapt to some degree. To invent a new species is a whole different ball game. Darwin theory has no explanation for it.

Genome complexity: variation within species

by David Turell @, Saturday, December 10, 2016, 23:56 (2666 days ago) @ David Turell

David’s comment: It is becoming recognized that alternate metabolic pathways may be present in many species, as I noted in our previous discussions about bacteria responding to antibiotics (can't find the reference). The species is still one species. It is not a new evolutionary process as the articles headline proclaim.

dhw: May I suggest that if the killifish is able to cope so quickly with different pollutants, what it carries before the sites are polluted is not an alternative metabolic pathway anticipating whatever might happen next, but the ability to process new information and change its genome accordingly – which means it can construct a new metabolic pathway to cope with each new threat.


David: On the other hand the article clearly suggests there are variable individuals in the species some of whom can handle the pollution and survive.

Another article on killfish supports my viewpoint:

https://www.newscientist.com/article/2115635-fish-rapidly-adapt-to-pollution-thousands-...

"The team found dozens of changes in the fish that have evolved to help them tolerate pollutants such as dioxins and PCBs. “We have a picture of the entire adaptive genetic type,” says Whitehead.

"Many of these changes are in genes involved in a signalling pathway that has several roles in normal killifish, including in the immune system and for oestrogen signalling.

"This so-called AHR pathway also kicks in to deal with natural toxins. But if the pathway is switched on by pollutants during early development, it causes havoc. “It really messes things up,” says Whitehead.

"All the pollution-tolerant fish have several changes in AHR-related genes that stop it kicking in at the wrong time. However, evolution has not taken the same route in each population. Pollution-tolerant fish from different areas have different mutations in these genes.

"In addition, there are many changes in other genes to compensate for those in the AHR pathway. Because of its multiple roles, mutations that stop it being activated have many knock-on effects.

"The areas in which the killifish live started becoming polluted in the 1950s, so all these evolutionary changes arose over just dozens of generations. It could happen so quickly, says Whitehead, because there was already a lot of variation in the species. “Killifish have insect-like levels of genetic diversity,” he says. (my bold)

"Wirgin thinks the fact that killifish are territorial also helps them evolve fast, because it means that those from polluted areas are less likely to dilute their genes by interbreeding with those from pristine ones.

"Although killifish have evolved to thrive even in polluted areas, not all animals are so adaptable. In particular, there is much less diversity in large animals with smaller populations, meaning they may not be able to evolve fast enough to cope with the abrupt changes resulting from human activities. This is why it is vital to conserve diversity, says Whitehead."

Comment: Note the bolded area. The emphasis is on initial variability within the species to allow these adaptations to occur so rapidly. As pollution appears the most adaptable live and create more progeny that can withstand the changing environment. Still the same species, but adapted to a severe challenge.

Genome complexity: variation within species

by dhw, Sunday, December 11, 2016, 13:06 (2665 days ago) @ David Turell

dhw: As always, a powerful case for design. But design of what? A microcosm within a macrocosm? “[…] It’s as if we are inhabited by a colony of ants, each with their own particular role to play, but constantly communicating, adapting, making decisions in the world that is you or me. It’s what some scientists call cellular intelligence.
DAVID: The design comes from the intelligent information in DNA. The entire design of the organism. The source of that information is what you and I debate.

I’m always queasy about the expression “intelligent information”, as it seems to me that intelligence either invents or uses information. But even if we accept it, one can argue that just as the “intelligent information” in the human brain autonomously produces its own designs, the intelligent information in cellular DNA does the same, redesigning itself and the rest of the cell/cell community.

dhw: May I suggest that if the killifish is able to cope so quickly with different pollutants, what it carries before the sites are polluted is not an alternative metabolic pathway anticipating whatever might happen next, but the ability to process new information and change its genome accordingly – which means it can construct a new metabolic pathway to cope with each new threat. And I would suggest that this applies to all processes of adaptation, though different organisms will have different capacities for change.

DAVID: On the other hand the article clearly suggests there are variable individuals in the species some of whom can handle the pollution and survive.

You are repeating precisely what I have just said, and what I repeat later: "But what is really interesting is the variability between individuals. This would explain how common descent works. Changes can only take place in individuals, and individuals are different. So some will respond to environmental change and others won’t. The same point is made in the second article you have quoted, and in my view fits in perfectly with the hypothesis that evolution is driven by individual intelligences.

Dhw: We don’t know how far the ability for change can extend. Or do you still think your God put each alternative metabolic pathway for all eventualities into the first cells to pass on to the killifish a few thousand million years later?
DAVID: Many species have variable individuals who can survive changes, nothing more.

That does not answer my question. We agree that some individuals are more adaptable than others. I have suggested that organisms are able to work out their own metabolic pathways. If you disagree, what is your alternative, if it is NOT divine preprogramming or dabbling?

dhw: So far we only know of adaptation and non-adaptation (those that can’t respond will die). But it is conceivable that the variation will also apply to innovation. Some organisms may have the wherewithal to invent. In much the same way as some humans are creative, and some are not.
DAVID: All organisms can adapt to some degree. To invent a new species is a whole different ball game. Darwin theory has no explanation for it.

Nobody can explain it. That is why we have different hypotheses: Darwin’s random mutations, David’s divine preprogramming/dabbling, and dhw’s cellular intelligence.

Genome complexity: variation within species

by David Turell @, Sunday, December 11, 2016, 19:24 (2665 days ago) @ dhw


DAVID: On the other hand the article clearly suggests there are variable individuals in the species some of whom can handle the pollution and survive.

dhw: You are repeating precisely what I have just said, and what I repeat later: "But what is really interesting is the variability between individuals. This would explain how common descent works. Changes can only take place in individuals, and individuals are different. So some will respond to environmental change and others won’t. The same point is made in the second article you have quoted, and in my view fits in perfectly with the hypothesis that evolution is driven by individual intelligences.

I am emphasizing individual differences in the variability in species, which means, as I pointed out in bacteria, some have alternate pathways already on board, or are partially immune to begin with. That means new adaptations don't have to be invented. Reproduction between partially immune or pollution resistant individuals will solve the issue as more fit individuals appear on the scene in a few generations.

Genome complexity: variation within species

by dhw, Monday, December 12, 2016, 15:40 (2664 days ago) @ David Turell

DAVID: On the other hand the article clearly suggests there are variable individuals in the species some of whom can handle the pollution and survive.

dhw: You are repeating precisely what I have just said, and what I repeat later: "But what is really interesting is the variability between individuals. This would explain how common descent works. Changes can only take place in individuals, and individuals are different. So some will respond to environmental change and others won’t. The same point is made in the second article you have quoted, and in my view fits in perfectly with the hypothesis that evolution is driven by individual intelligences.

DAVID: I am emphasizing individual differences in the variability in species, which means, as I pointed out in bacteria, some have alternate pathways already on board, or are partially immune to begin with. That means new adaptations don't have to be invented. Reproduction between partially immune or pollution resistant individuals will solve the issue as more fit individuals appear on the scene in a few generations.

I am also talking about individual differences in the variability in species, because both adaptations and innovations must take place in individuals. The number of threats to bacterial existence must be absolutely colossal, since they are able to adapt to so many different environments. Your theory therefore demands that they have the same number of “alternate pathways” (not alternative?) on board. So your God has provided them with all these pathways, and without knowing what they’re doing, they simply switch on the correct one when they encounter the appropriate change in conditions? And as I have asked before, what is the use of partial immunity? Does it enable them to be just partially dead? Why is your theory more likely than the hypothesis that some individuals are able to work out a counter to the threat, and then “reproduction between immune or pollution resistant individuals will solve the issue as more fit individuals appear on the scene in a few generations”?

Genome complexity: variation within species

by David Turell @, Monday, December 12, 2016, 17:33 (2664 days ago) @ dhw


DAVID: I am emphasizing individual differences in the variability in species, which means, as I pointed out in bacteria, some have alternate pathways already on board, or are partially immune to begin with. That means new adaptations don't have to be invented. Reproduction between partially immune or pollution resistant individuals will solve the issue as more fit individuals appear on the scene in a few generations.

dhw:I am also talking about individual differences in the variability in species, because both adaptations and innovations must take place in individuals.

Of course we are discussing individuals, who are variable and have differing strengths to handle increasing pollution levels. The strong ones reproduce and survive and their progeny survive. Why is that so hard to understand?

dhw: Why is your theory more likely than the hypothesis that some individuals are able to work out a counter to the threat, and then “reproduction between immune or pollution resistant individuals will solve the issue as more fit individuals appear on the scene in a few generations”?

Because what I have described is the accepted explanation for resistance.

Genome complexity: variation within species

by dhw, Tuesday, December 13, 2016, 12:52 (2663 days ago) @ David Turell

DAVID: I am emphasizing individual differences in the variability in species, which means, as I pointed out in bacteria, some have alternate pathways already on board, or are partially immune to begin with. That means new adaptations don't have to be invented. Reproduction between partially immune or pollution resistant individuals will solve the issue as more fit individuals appear on the scene in a few generations.

dhw:I am also talking about individual differences in the variability in species, because both adaptations and innovations must take place in individuals.

DAVID: Of course we are discussing individuals, who are variable and have differing strengths to handle increasing pollution levels.

Precisely.

DAVID: The strong ones reproduce and survive and their progeny survive. Why is that so hard to understand?

I said exactly the same, using your own words, in my very next sentence:

dhw: Why is your theory more likely than the hypothesis that some individuals are able to work out a counter to the threat, and then “reproduction between immune or pollution resistant individuals will solve the issue as more fit individuals appear on the scene in a few generations”?

DAVID: Because what I have described is the accepted explanation for resistance.

What part of your theory is “accepted”? That your God provided alternative pathways for the first cells to pass on to bacteria, so that in a million different situations some of them would be able to resist the new threat to their existence by switching onto the correct pathway without knowing what they were doing? What is accepted is that bacteria find answers to countless problems. Scientists can analyse the answers, which of course are physical since the problems are also physical. What they cannot analyse is how the bacteria come up with those answers. You propose that your God preprogrammed them to do so automatically. I propose that they have the intelligence (perhaps God-given) to work out each new programme. You have said yourself that nobody can tell the difference from outside, and nobody can get inside. 50/50.

Genome complexity: variation within species

by David Turell @, Tuesday, December 13, 2016, 19:40 (2663 days ago) @ dhw


DAVID: Because what I have described is the accepted explanation for resistance.

dhw: What part of your theory is “accepted”?

That bacteria come with alternative pathways built-in that can be employed when necessary. And that individual variation allows for some individuals to be more immune or resistant to noxious changes that they survive, reproduce and create a group that is more prepared to handle the challenges and changes.

dhW: That your God provided alternative pathways for the first cells to pass on to bacteria, so that in a million different situations some of them would be able to resist the new threat to their existence by switching onto the correct pathway without knowing what they were doing?

The pathways exist. God or not.

dhw: What is accepted is that bacteria find answers to countless problems. Scientists can analyse the answers, which of course are physical since the problems are also physical. What they cannot analyse is how the bacteria come up with those answers. You propose that your God preprogrammed them to do so automatically. I propose that they have the intelligence (perhaps God-given) to work out each new programme. You have said yourself that nobody can tell the difference from outside, and nobody can get inside. 50/50.

We remain apart.

Genome complexity: variation within species

by dhw, Wednesday, December 14, 2016, 13:54 (2662 days ago) @ David Turell

DAVID: Because what I have described is the accepted explanation for resistance.
dhw: What part of your theory is “accepted”?
DAVID: That bacteria come with alternative pathways built-in that can be employed when necessary. And that individual variation allows for some individuals to be more immune or resistant to noxious changes that they survive, reproduce and create a group that is more prepared to handle the challenges and changes.

No question that individuals are different: that has been at the very core of my evolutionary hypothesis – that each adaptation and innovation must take place in individuals, and this means that there is no overall programme, but both processes depend on the ”intelligence” of the individual. The argument that alternative pathways are “built into” some organisms (though not into others) simply boils down to saying that whenever a problem is solved, that proves there is a solution, and so the potential solution existed before the problem arose. The same would apply to inventions. If something new can be created, the potential for the something new was already there. If you wish to adopt that approach, I would argue that it requires intelligence to find the solution/realize the potential.

dhW: ...That your God provided alternative pathways for the first cells to pass on to bacteria, so that in a million different situations some of them would be able to resist the new threat to their existence by switching onto the correct pathway without knowing what they were doing?
DAVID: The pathways exist. God or not.

See above. But if you insist that bacteria are programmed to find the right pathway (since you believe they are automatons), what alternative do you have to the claim that your God must have preprogrammed the first cells to pass on solutions to every single problem that bacteria might encounter throughout the history of life?

Genome complexity: variation within species

by David Turell @, Wednesday, December 14, 2016, 18:20 (2662 days ago) @ dhw

DAVID: That bacteria come with alternative pathways built-in that can be employed when necessary. And that individual variation allows for some individuals to be more immune or resistant to noxious changes that they survive, reproduce and create a group that is more prepared to handle the challenges and changes.

dhw: No question that individuals are different: that has been at the very core of my evolutionary hypothesis – that each adaptation and innovation must take place in individuals, and this means that there is no overall programme, but both processes depend on the ”intelligence” of the individual.

With variation and with alternative pathways, the adaptations may be relatively automatic, relatively if partially resistant organisms have to have several generations to arrive at complete resistance.

dhw: The argument that alternative pathways are “built into” some organisms (though not into others) simply boils down to saying that whenever a problem is solved, that proves there is a solution, and so the potential solution existed before the problem arose. The same would apply to inventions. If something new can be created, the potential for the something new was already there. If you wish to adopt that approach, I would argue that it requires intelligence to find the solution/realize the potential.

Shifting to an alternative pathway can easily be automatic, not intelligent.


dhW: ...That your God provided alternative pathways for the first cells to pass on to bacteria, so that in a million different situations some of them would be able to resist the new threat to their existence by switching onto the correct pathway without knowing what they were doing?
DAVID: The pathways exist. God or not.

dhw: See above. But if you insist that bacteria are programmed to find the right pathway (since you believe they are automatons), what alternative do you have to the claim that your God must have preprogrammed the first cells to pass on solutions to every single problem that bacteria might encounter throughout the history of life?

Generally no alternative except dabbling which we have discussed.

Genome complexity: variation within species

by David Turell @, Wednesday, December 14, 2016, 23:59 (2662 days ago) @ David Turell

I introduced the story about killfish on Dec. 9th and their rapid development of resistance to pollution. Here is another take, supporting my thought that the way to protection was already present:

https://www.washingtonpost.com/news/speaking-of-science/wp/2016/12/08/these-fish-evolve...

:But under ordinary circumstances, they struggle to cope with environmental pollutants: If you dropped an average killifish into toxic waters, it wouldn't last very long.

"That's why ecologists have puzzled over the populations that persist in the Elizabeth River, as well as in New Bedford Harbor in Massachusetts, the waters around Bridgeport, Conn., and New Jersey's Newark Bay — all former industrial sites now on the Superfund list. The fish there are able to withstand levels of pollution 8,000 times higher than the normal lethal limit. Clearly, they've had some adaptation that the rest of their species lacked. What was it?

"To find out, Whitehead and his colleagues sequenced the genomes of nearly 400 killifish from those four spots and four non-polluted areas nearby. The fish from the Superfund sites shared a set of mutations on a part of the genome related to a signaling pathway called aryl hydrocarbon receptor (AHR). The pathway regulates the immune system and release of the hormone estrogen, and, most importantly, it mediates toxicity. It's what makes killifish sensitive to pollutants. But without AHR, they can swim in toxic waters without getting hurt. 

"It's unusual for animals like killifish — which have life spans of years, not months — to evolve so rapidly, especially in four separate spots. To Whitehead, that suggests the mutation for the AHR deletion already existed in the larger killifish population, lying dormant like a superpower the animals didn't know they had. Once the changing environmental circumstances made the mutation useful for fish in polluted spots, it rapidly spread to the rest of the community. In real time, the animals evolved to adapt to their poisoned habitat. (my bold)

***

"When environmental shifts happen fast, animals can't wait around for the right, helpful mutation to occur, especially if they're animals with long life spans that don't reproduce very rapidly. They have to hope that this mutation already exists in the population, waiting to become useful.

"The latter scenario is more likely to happen when the population in question is larger and thus contains a larger degree of genetic diversity. The killifish population is one of the biggest.

“'Killifish top the charts in terms of vertebrates,” Whitehead said. “That’s probably what stacked the deck in their favor.”

"The situation holds a certain “tragic irony,” he said. Species that harbor large numbers of organisms and huge amounts of genetic diversity — think bugs and bacteria — are most able to adapt to new and deadly poisons. Unfortunately, those are usually the species that we're trying to tamp down. Meanwhile, populations humans hope to save, because they've been decimated by hunting or habitat loss, are least equipped to evolve.

“'There’s a critical level of genetic diversity that's necessary for the adaptive potential of species,” he continued. Most endangered species, by virtue of being endangered, don't have it." (my bold)

Comment: Please read my bolded areas especially. This supports my contention that challenged surviving species have original genetic diversity to help them survive. No inventions involved.

Genome complexity: variation within species

by dhw, Thursday, December 15, 2016, 16:59 (2661 days ago) @ David Turell

QUOTES: It's unusual for animals like killifish — which have life spans of years, not months — to evolve so rapidly, especially in four separate spots. To Whitehead, that suggests the mutation for the AHR deletion already existed in the larger killifish population, lying dormant like a superpower the animals didn't know they had. Once the changing environmental circumstances made the mutation useful for fish in polluted spots, it rapidly spread to the rest of the community. In real time, the animals evolved to adapt to their poisoned habitat.[/b] (David's bold)

'There’s a critical level of genetic diversity that's necessary for the adaptive potential of species,” he continued. Most endangered species, by virtue of being endangered, don't have it." (David's bold)

David’s comment: Please read my bolded areas especially. This supports my contention that challenged surviving species have original genetic diversity to help them survive. No inventions involved.

All perfectly logical, including the fact that no invention is involved in adaptation. It is innovation that leads to speciation, and nobody can explain that. Potential is the key word. The potential for the life-saving mutation must have been there, or the killifish couldn’t have survived. And there is obviously genetic diversity, or every species would survive. This means that individuals and species are all different, with different potentials. How do they fulfil their different potentials? According to you, through programmes handed down by the very first cells, or by God personally intervening. My (theistic) alternative is that your God gave individuals the ability to use whatever potential they have, and potentials themselves continued to develop as cell communities devised more and more ways of coping with or exploiting the environment. We see the same process in human history, as generations build on the achievements of their predecessors. In my view, this is also perfectly logical.

Genome complexity: variation within species

by David Turell @, Thursday, December 15, 2016, 19:39 (2661 days ago) @ dhw

QUOTES: It's unusual for animals like killifish — which have life spans of years, not months — to evolve so rapidly, especially in four separate spots. To Whitehead, that suggests the mutation for the AHR deletion already existed in the larger killifish population, lying dormant like a superpower the animals didn't know they had. Once the changing environmental circumstances made the mutation useful for fish in polluted spots, it rapidly spread to the rest of the community. In real time, the animals evolved to adapt to their poisoned habitat.[/b] (David's bold)

'There’s a critical level of genetic diversity that's necessary for the adaptive potential of species,” he continued. Most endangered species, by virtue of being endangered, don't have it." (David's bold)

David’s comment: Please read my bolded areas especially. This supports my contention that challenged surviving species have original genetic diversity to help them survive. No inventions involved.

dhw: All perfectly logical, including the fact that no invention is involved in adaptation. It is innovation that leads to speciation, and nobody can explain that. Potential is the key word. The potential for the life-saving mutation must have been there, or the killifish couldn’t have survived. And there is obviously genetic diversity, or every species would survive. This means that individuals and species are all different, with different potentials. How do they fulfil their different potentials? According to you, through programmes handed down by the very first cells, or by God personally intervening. My (theistic) alternative is that your God gave individuals the ability to use whatever potential they have, and potentials themselves continued to develop as cell communities devised more and more ways of coping with or exploiting the environment.

If bacteria, the initial life forms, are extremely variable within species as shown in this article I presented on Dec. 9th: Friday, December 09, 2016, 18:51,

http://www.the-scientist.com/?articles.view/articleNo/47510/title/The-Pangenome--Are-Si...

why not accept that the variability was supplied by God from the beginning? They obviously use the 'toolkit' easily as the article describes and can live anywhere/everywhere as we see. They didn't have to 'devise' much, if anything, with the tools they were given originally. You are right. All existing potential!

Genome complexity: variation within species

by dhw, Thursday, December 15, 2016, 16:47 (2661 days ago) @ David Turell

dhw: No question that individuals are different: that has been at the very core of my evolutionary hypothesis – that each adaptation and innovation must take place in individuals, and this means that there is no overall programme, but both processes depend on the ”intelligence” of the individual.
DAVID: With variation and with alternative pathways, the adaptations may be relatively automatic, relatively if partially resistant organisms have to have several generations to arrive at complete resistance.

A nice bit of Darwinian itty-bitty improvement. Do partially resistant organisms just die more slowly? I don’t understand what you mean by “relatively automatic”. The expression has nothing to do with a gradually improved resistance. Either the process is completely automatic or organisms take decisions of their own.

dhw: The argument that alternative pathways are “built into” some organisms (though not into others) simply boils down to saying that whenever a problem is solved, that proves there is a solution, and so the potential solution existed before the problem arose. The same would apply to inventions. If something new can be created, the potential for the something new was already there. If you wish to adopt that approach, I would argue that it requires intelligence to find the solution/realize the potential.
DAVID: Shifting to an alternative pathway can easily be automatic, not intelligent.

And it can easily be intelligent and not automatic. 50/50. But see below.

dhw: … if you insist that bacteria are programmed to find the right pathway (since you believe they are automatons), what alternative do you have to the claim that your God must have preprogrammed the first cells to pass on solutions to every single problem that bacteria might encounter throughout the history of life?DAVID: Generally no alternative except dabbling which we have discussed.

Thank you. That is the nub of the matter. According to you, the first cells contained and passed on programmes for millions of solutions for bacteria, millions of innovations, millions of lifestyles and natural wonders. The only alternative is God intervening every time bacteria have a problem. Your article on killifish raises the same issue: your God provided the first cells with all the different pathways necessary for the killifish to resist pollutants (but to hell with those species that perish) – or each time he sees the killifish under threat, he steps in. I wonder why the killifish is so much more important to God than the fish that perish. Impossible for humans to exist without killifish?

Genome complexity: variation within species

by David Turell @, Thursday, December 15, 2016, 20:23 (2661 days ago) @ dhw

DAVID: With variation and with alternative pathways, the adaptations may be relatively automatic, relatively if partially resistant organisms have to have several generations to arrive at complete resistance.

dhw: A nice bit of Darwinian itty-bitty improvement. Do partially resistant organisms just die more slowly? I don’t understand what you mean by “relatively automatic”. The expression has nothing to do with a gradually improved resistance. Either the process is completely automatic or organisms take decisions of their own.

See my other entry on the subject today with the reference article. Some partially resistant organisms survive and reproduce more resistant progeny until the existing population is fully resistant, just as in the E. coli antibiotic resistance discussion we had. The 'partially automatic' refers to the reproductive process which takes several generations to work.

dhw: … if you insist that bacteria are programmed to find the right pathway (since you believe they are automatons), what alternative do you have to the claim that your God must have preprogrammed the first cells to pass on solutions to every single problem that bacteria might encounter throughout the history of life?

DAVID: Generally no alternative except dabbling which we have discussed.


dhw: Thank you. That is the nub of the matter. According to you, the first cells contained and passed on programmes for millions of solutions for bacteria, millions of innovations, millions of lifestyles and natural wonders. The only alternative is God intervening every time bacteria have a problem. Your article on killifish raises the same issue: your God provided the first cells with all the different pathways necessary for the killifish to resist pollutants (but to hell with those species that perish) – or each time he sees the killifish under threat, he steps in. I wonder why the killifish is so much more important to God than the fish that perish. Impossible for humans to exist without killifish?

I doubt there was any need for dabbling here. Their variability gave them a way out of extinction through reproduction by the partially resistant.

Genome complexity: variation within species

by dhw, Friday, December 16, 2016, 12:10 (2660 days ago) @ David Turell

DAVID: If bacteria, the initial life forms, are extremely variable within species as shown in this article I presented on Dec. 9th: Friday, December 09, 2016, 18:51,
http://www.the-scientist.com/?articles.view/articleNo/47510/title/The-Pangenome--Are-Si...
why not accept that the variability was supplied by God from the beginning? They obviously use the 'toolkit' easily as the article describes and can live anywhere/everywhere as we see. They didn't have to 'devise' much, if anything, with the tools they were given originally. You are right. All existing potential!

I have always allowed for the possibility that God supplied the toolkit from the beginning. But what is central to my overall evolutionary hypothesis is that they do “use” it. They are not preprogrammed, and some are better than others at using it(= variability). And that is where “intelligence” comes in.

DAVID: With variation and with alternative pathways, the adaptations may be relatively automatic, relatively if partially resistant organisms have to have several generations to arrive at complete resistance.

dhw: A nice bit of Darwinian itty-bitty improvement. Do partially resistant organisms just die more slowly? I don’t understand what you mean by “relatively automatic”. The expression has nothing to do with a gradually improved resistance. Either the process is completely automatic or organisms take decisions of their own.
DAVID: See my other entry on the subject today with the reference article. Some partially resistant organisms survive and reproduce more resistant progeny until the existing population is fully resistant, just as in the E. coli antibiotic resistance discussion we had. The 'partially automatic' refers to the reproductive process which takes several generations to work.

I still don’t understand partial resistance, but you are the expert. I’d have thought organisms which survive are resistant, and the resistant organisms reproduce while the non-resistant ones die, so that in the end you have a fully existing population of resistant organisms. And I’d have thought that the initially resistant ones were the individuals which were best able to use the ‘toolkit’ your God may have provided them with at the beginning: namely, the intelligence with which to work out their own methods of survival.

Genome complexity: variation within species

by David Turell @, Friday, December 16, 2016, 15:28 (2660 days ago) @ dhw


dhw: I have always allowed for the possibility that God supplied the toolkit from the beginning. But what is central to my overall evolutionary hypothesis is that they do “use” it. They are not preprogrammed, and some are better than others at using it(= variability). And that is where “intelligence” comes in.

And I’d have thought that the initially resistant ones were the individuals which were best able to use the ‘toolkit’ your God may have provided them with at the beginning: namely, the intelligence with which to work out their own methods of survival.

What you call intelligence is the presence of alternative metabolic pathways. If one is not working the organism, the next is switched on, nothing more.

Genome complexity: variation within species

by dhw, Saturday, December 17, 2016, 13:26 (2659 days ago) @ David Turell

dhw: I have always allowed for the possibility that God supplied the toolkit from the beginning. But what is central to my overall evolutionary hypothesis is that they do “use” it. They are not preprogrammed, and some are better than others at using it(= variability). And that is where “intelligence” comes in.

And I’d have thought that the initially resistant ones were the individuals which were best able to use the ‘toolkit’ your God may have provided them with at the beginning: namely, the intelligence with which to work out their own methods of survival.

DAVID: What you call intelligence is the presence of alternative metabolic pathways. If one is not working the organism, the next is switched on, nothing more.

What switches it on, and why is it switched on in some but not in others if your God made the mechanism automatic?

Genome complexity: variation within species

by David Turell @, Saturday, December 17, 2016, 14:38 (2659 days ago) @ dhw


DAVID: What you call intelligence is the presence of alternative metabolic pathways. If one is not working the organism, the next is switched on, nothing more.

dhw: What switches it on, and why is it switched on in some but not in others if your God made the mechanism automatic?

Organisms have the ability to use whatever metabolic pathways are available within them. With species variability, not all organisms in the species have the same pathways onboard, which is why some are partially or fully immune/resistant and some are not. And remember horizontal gene transfer is also present primarily in bacteria.

Genome complexity: variation within species

by dhw, Sunday, December 18, 2016, 13:22 (2658 days ago) @ David Turell

DAVID: What you call intelligence is the presence of alternative metabolic pathways. If one is not working the organism, the next is switched on, nothing more.

dhw: What switches it on, and why is it switched on in some but not in others if your God made the mechanism automatic?

DAVID: Organisms have the ability to use whatever metabolic pathways are available within them. With species variability, not all organisms in the species have the same pathways onboard, which is why some are partially or fully immune/resistant and some are not. And remember horizontal gene transfer is also present primarily in bacteria.

Intelligent organisms - including humans – have the ability to use whatever pathways are available to them. With species variability, not all organisms in the species – including humans – have the same pathways on board, which is why some are more intelligent than others. And remember that such manifestations of intelligence as communication and cooperation and information-processing and decision-making are integral to the behaviour even of bacteria.

Genome complexity: variation within species

by David Turell @, Sunday, December 18, 2016, 21:37 (2658 days ago) @ dhw

dhw: And remember that such manifestations of intelligence as communication and cooperation and information-processing and decision-making are integral to the behaviour even of bacteria.

Remember what bacteria are using is intelligently designed information, from the beginning of life.

Genome complexity: variation within species

by dhw, Monday, December 19, 2016, 12:46 (2657 days ago) @ David Turell

dhw: And remember that such manifestations of intelligence as communication and cooperation and information-processing and decision-making are integral to the behaviour even of bacteria.

DAVID: Remember what bacteria are using is intelligently designed information, from the beginning of life.

How do you tell the difference between “intelligently designed information” and autonomous intelligence, which your God may have provided “from the beginning of life”?

Genome complexity: variation within species

by David Turell @, Monday, December 19, 2016, 15:24 (2657 days ago) @ dhw

dhw: And remember that such manifestations of intelligence as communication and cooperation and information-processing and decision-making are integral to the behaviour even of bacteria.

DAVID: Remember what bacteria are using is intelligently designed information, from the beginning of life.

dhw: How do you tell the difference between “intelligently designed information” and autonomous intelligence, which your God may have provided “from the beginning of life”?

My same old point. From the outside, the odds are 50/50, but with research on the inside what is found are automatic molecular responses to stimuli and reactions, n nothing more. A kidney excretory cell balances salt levels in the body and fluid balance while creating urine, which content is variable depending upon need. All totally automatic. Bacteria are no different in mechanisms observed.

Genome complexity: variation within species

by David Turell @, Monday, December 19, 2016, 23:46 (2657 days ago) @ David Turell

A new discovery is that some survivors of antibiotics simple have a mechanism rto go dormant until the danger is over:

https://www.sciencedaily.com/releases/2016/12/161219161610.htm

"A new publication from the BASP Centre, University of Copenhagen now presents how even sensitive bacteria often manage to survive antibiotic treatment as so-called 'persister cells'. The comprehensive perspective on this phenomenon may help to improve current options of drug treatment and could even inspire the discovery of novel antibiotics targeting these notoriously difficult-to-treat persister bacteria.

"In the current issue of the journal Science, Alexander Harms and colleagues from the BASP Centre, Department of Biology, University of Copenhagen summarise newly discovered molecular mechanisms explaining how bacteria manage to survive antibiotic treatment and cause chronic and recurrent infections.

"Post-Doc Alexander Harms explains: "This amazing resilience is often due to hibernation in a physiological state called persistence where the bacteria are tolerant to multiple antibiotics and other stressors. Bacterial cells can switch into persistence by activating dedicated physiological programs that literally pull the plug of important cellular processes. Once they are persisters, the bacteria may sit through even long-lasting antibiotic therapy and can resuscitate to cause relapsing infections at any time after the treatment is abandoned." (my bold)

"Using novel detection methods, recent work in the field has uncovered the molecular architecture of several cellular pathways underlying the formation of bacterial persisters -- and these results confirmed the long-standing notion that persistence is intimately connected to slow growth or dormancy. Bacterial persistence can therefore be compared to hibernation of animals or the durable spores produced by many mushrooms and plants.

"Across many different bacteria, these programs are controlled by a regulatory compound known as "magic spot" that plays a central role in the persistence phenomenon." (my bold)

Comment: My bolded areas show the automatic molecular controls that shift metabolism to alternate pathways. The term 'regulatory compound' is quite specific.

Genome complexity: variation within species

by dhw, Tuesday, December 20, 2016, 12:40 (2656 days ago) @ David Turell

DAVID: Remember what bacteria are using is intelligently designed information, from the beginning of life.
dhw: How do you tell the difference between “intelligently designed information” and autonomous intelligence, which your God may have provided “from the beginning of life”?
DAVID: My same old point. From the outside, the odds are 50/50, but with research on the inside what is found are automatic molecular responses to stimuli and reactions, n nothing more.

And my same old reply: This also applies to what is found inside the human brain. You cannot see the intelligence that gives rise to thought that gives rise to action. You can only see the molecular responses.

DAVID: A kidney excretory cell balances salt levels in the body and fluid balance while creating urine, which content is variable depending upon need. All totally automatic. Bacteria are no different in mechanisms observed.

And another same old: you always pick on an established organ which HAS to perform its function automatically because otherwise it won’t work. The point of my cellular intelligence hypothesis is to explain evolutionary INNOVATION, not what happens once the organ has been invented. As for bacteria, same old same old: the only way you can test whether they are intelligent is to set them new problems, which some experts have done, drawing the conclusion that they are intelligent.

xxxxxxxx

DAVID: A new discovery is that some survivors of antibiotics simple have a mechanism to go dormant until the danger is over:

https://www.sciencedaily.com/releases/2016/12/161219161610.htm

QUOTES: Post-Doc Alexander Harms explains: "This amazing resilience is often due to hibernation in a physiological state called persistence where the bacteria are tolerant to multiple antibiotics and other stressors. Bacterial cells can switch into persistence by activating dedicated physiological programs that literally pull the plug of important cellular processes. Once they are persisters, the bacteria may sit through even long-lasting antibiotic therapy and can resuscitate to cause relapsing infections at any time after the treatment is abandoned." (David’s bold)
"Bacterial persistence can therefore be compared to hibernation of animals or the durable spores produced by many mushrooms and plants.
"Across many different bacteria, these programs are controlled by a regulatory compound known as "magic spot" that plays a central role in the persistence phenomenon
." (David’s bold)

David’s comment: My bolded areas show the automatic molecular controls that shift metabolism to alternate pathways. The term 'regulatory compound' is quite specific.

Same argument. Of course there have to be physical controls to adapt the body to physical threats. Some bacteria have them, some don’t. In all areas of life you have some individuals that have worked out how to solve problems, and others that haven’t. Successful solutions get passed on. I like the comparison with hibernation. That is also a method by which certain organisms are able to counter the threat of a hostile environment by “shifting their metabolism”. How did it ORIGINATE? Your God preprogramming or dabbling it in order to produce humans? Or your God (theistic version)) giving organisms the intelligence to work it out for themselves?

Genome complexity: variation within species

by David Turell @, Tuesday, December 20, 2016, 16:11 (2656 days ago) @ dhw

DAVID: My same old point. From the outside, the odds are 50/50, but with research on the inside what is found are automatic molecular responses to stimuli and reactions, n nothing more.

dhw:And my same old reply: This also applies to what is found inside the human brain. You cannot see the intelligence that gives rise to thought that gives rise to action. You can only see the molecular responses.

Apples and oranges. I am discussing demonstrable material actions and you are bringing in immaterial consciousness. Whew!


dhw: As for bacteria, same old same old: the only way you can test whether they are intelligent is to set them new problems, which some experts have done, drawing the conclusion that they are intelligent.

Since bacteria started so long ago and faced every6 possible threat, all their survival mechanisms had to be present from the beginning.


xxxxxxxx
David’s comment: My bolded areas show the automatic molecular controls that shift metabolism to alternate pathways. The term 'regulatory compound' is quite specific. >

shw: Same argument. Of course there have to be physical controls to adapt the body to physical threats. Some bacteria have them, some don’t. In all areas of life you have some individuals that have worked out how to solve problems, and others that haven’t. Successful solutions get passed on. I like the comparison with hibernation. That is also a method by which certain organisms are able to counter the threat of a hostile environment by “shifting their metabolism”. How did it ORIGINATE? Your God preprogramming or dabbling it in order to produce humans? Or your God (theistic version)) giving organisms the intelligence to work it out for themselves?

Same response. Life at the beginning faced all sorts of immediate dangers. They had to have protection from the beginning.

Genome complexity: variation within species

by dhw, Wednesday, December 21, 2016, 17:48 (2655 days ago) @ David Turell

DAVID: My same old point. From the outside, the odds are 50/50, but with research on the inside what is found are automatic molecular responses to stimuli and reactions, n nothing more.

dhw:And my same old reply: This also applies to what is found inside the human brain. You cannot see the intelligence that gives rise to thought that gives rise to action. You can only see the molecular responses.

DAVID: Apples and oranges. I am discussing demonstrable material actions and you are bringing in immaterial consciousness. Whew!

Of course I am bringing in immaterial consciousness! That is the whole basis of our disagreement. Let me spell it out for you: if bacteria are intelligent, as Shapiro et al claim, researchers will still only be able to study the molecular reactions, because consciousness/intelligence is immaterial or undemonstrable. Put it another way: neuroscientists can observe demonstrable molecular responses in the human brain, but they cannot observe consciousness. The fact that you cannot study something materially does not mean it is not there.

dhw: As for bacteria, same old same old: the only way you can test whether they are intelligent is to set them new problems, which some experts have done, drawing the conclusion that they are intelligent.

DAVID: Since bacteria started so long ago and faced every possible threat, all their survival mechanisms had to be present from the beginning.

Agreed. In my hypothesis, the survival mechanism would consist in their “plasticity” and the intelligence to work out how to use it in solving the problems posed by each individual threat. Some succeed and some don’t. Your hypothesis has your God preprogramming the first cells to pass on “all the alternative pathways they need for any crisis from the beginning” (see under “big brain evolution”), which I take to mean every solution to every problem. Not very efficient programming if some succeed and some don’t. Does he also select the successful bacteria, or leave that to chance?

Genome complexity: variation within species

by David Turell @, Wednesday, December 21, 2016, 20:58 (2655 days ago) @ dhw

DAVID: Since bacteria started so long ago and faced every possible threat, all their survival mechanisms had to be present from the beginning.

dhw: Agreed. In my hypothesis, the survival mechanism would consist in their “plasticity” and the intelligence to work out how to use it in solving the problems posed by each individual threat. Some succeed and some don’t. Your hypothesis has your God preprogramming the first cells to pass on “all the alternative pathways they need for any crisis from the beginning” (see under “big brain evolution”), which I take to mean every solution to every problem. Not very efficient programming if some succeed and some don’t. Does he also select the successful bacteria, or leave that to chance?

I think all the proper defense mechanisms were onboard from the beginning. Bacteria have adapted to everywhere.

Genome complexity: variation within species

by dhw, Thursday, December 22, 2016, 12:52 (2654 days ago) @ David Turell

DAVID: Since bacteria started so long ago and faced every possible threat, all their survival mechanisms had to be present from the beginning.

dhw: Agreed. In my hypothesis, the survival mechanism would consist in their “plasticity” and the intelligence to work out how to use it in solving the problems posed by each individual threat. Some succeed and some don’t. Your hypothesis has your God preprogramming the first cells to pass on “all the alternative pathways they need for any crisis from the beginning” (see under “big brain evolution”), which I take to mean every solution to every problem. Not very efficient programming if some succeed and some don’t. Does he also select the successful bacteria, or leave that to chance?

DAVID: I think all the proper defense mechanisms were onboard from the beginning. Bacteria have adapted to everywhere.

I have already agreed, and have explained above what I mean by defence/survival mechanisms, and what I think you mean by defence/survival mechanisms, and why I have certain difficulties with your concept.

Genome complexity:does variation in species drive evolution?

by David Turell @, Monday, September 20, 2021, 17:34 (921 days ago) @ dhw

Using fruit fly wing comparisons, not much:

https://www.quantamagazine.org/mathematical-analysis-of-fruit-fly-wings-hints-at-evolut...

"Persevering until they had perfectly mounted about 2,000 pairs, the scientists then photographed the wings in high resolution and systematically compared the photos in 30,000 places.

"This was no mere exercise in taxonomy. Rather, the study, which was recently published in the journal eLife, has offered an exceptionally detailed look at the variation that can exist within a species. The results begin to resolve a long-standing tension in biology.

"On one hand, despite dramatic mutations in individuals’ genes and diverse environments in which they grow, members of a species develop into strikingly similar creatures. This robustness ensures that almost all individuals are functional. On the other hand, for evolution to occur, members of a species need diverse traits that natural selection can act upon. Those two forces — robustness and evolvability — tug in opposite directions. One wants less variation, and one wants more.

***

"Unexpected simplicity emerged from this rich data. The scientists saw a narrow range of possible appearances for the wings, which mostly diverged in a small set of characteristics. The variation was concentrated near the hinge of the wing and showed up in a few particular spots, such as the shape of the frontmost vein. Moreover, these variable traits were linked: When one of the traits on a wing was far from the average, the other traits usually were, too. This was true no matter which genetic or environmental modifications that fly experienced, implying that these factors individually have very limited influence.

***

"The photos of fly wings offered no clues as to the mechanisms that restrict the possible morphologies that can develop. Rather, the results substantiated the extensive power of these guardrails. Natural selection must mostly act on the significant diversity exhibited in the small number of linked, variable traits, while robustness tightly constrains the rest."

comment: variation in fruit fly's wings is tiny. Darwin theory demands enough variation to allow evolution to advance to more complex forms. If the variations are this tiny, Darwin's theory is constrained. Small species adaptations are changes in degree. A completely new species is a change in kind. That possibility requires new design, not offered by the small variations seen in this study .

Genome complexity: Controlling 3-D DNA relationships

by David Turell @, Tuesday, September 21, 2021, 18:56 (920 days ago) @ David Turell

Special controls must be in place to open up specific genes to act:

https://phys.org/news/2021-09-proteins-symphonies-genes-statistical-theory.html

"'Many scholars at the crossroad between physics and biology are now approaching what is probably the most crucial puzzle of biology," said co-author Alessandro Giuliani. "How is it possible that, starting from the same genetic background in the fertilized egg, around 400 highly differentiated cell types can arise, each endowed with a specific physiological role?"

"Biology-based theories often center on regulator proteins, called transcription factors, that biochemically conduct a symphony of genes to be expressed together. By contrast, many physicists have focused on expression waves, the rhythmic changes in expression levels across the genome, driven by relaxation and condensing of the DNA molecule itself.

"'It is something like the so-called hola, common in soccer and in other sport events, in which the spectators stand up simultaneously giving rise to a 'wave' spreading all over the stadium," Giuliani said.

"To get at the heart of the issue, the group focuses on a specific type of cell found in breast cancer with a proven track record of consistently behaving the same way to stimuli.

"They used statistical mechanics to make sense of how DNA molecules fold by assessing the collective behavior of a huge number of microscopic players in terms of ensemble properties, unlike classical top-down perspectives, like Newton's laws.

"Ultimately, the researchers landed in favor of expression waves, acknowledging that while transcription factors play a vital role, they are second fiddle to the changing shape of DNA."

Comment: Not yet fully understood, but it shows the point that DNA is not just a protein-producing code but by having its shape adjusted many possible results are produced. Only exquisite design by a designer can create this.

Genome complexity: Controlling 3-D DNA relationships

by David Turell @, Wednesday, September 22, 2021, 18:33 (919 days ago) @ David Turell

New controls found:

https://phys.org/news/2021-09-insights-klf4-gene.html

"The study, published in the journal Nature Communications, reveals that the binding of KLF4 can cause DNA to condense into a separate liquid phase in a process called biomolecular condensation, which recruits other factors that influence gene expression.

"'Cells regulate the expression of their genes with proteins called transcription factors," said co-corresponding author Dr. Josephine C. Ferreon, assistant professor of pharmacology and chemical biology and member of the Dan L Duncan Comprehensive Cancer Center at Baylor. "In the current study, we focused on master transcription factor KLF4, which is known to selectively mediate gene expression and reprogramming that determines cell fate."

***

"'Imagine mixing oil and water, how they form separate layers, or two liquid phases," Ferreon said. "When KLF4 interacts with specific chromatin regions, it forms a condensate—a separate liquid phase—that preferentially recruits other molecules that help open the chromatin and mediate gene transcription."

"Other transcription factors participate in biomolecular condensation through unstructured protein regions, but the researchers showed that KLF4 droplets form in cells even if its unstructured regions are not present. Instead, KLF4 droplet formation depends on regions called zinc fingers, which are known to bind DNA. Single molecule fluorescence experiments show that the three KLF4 zinc fingers, which usually bind in a row to one DNA, can 'bridge' between two DNA molecules.

"'This type of biomolecular condensation involving zinc fingers and DNA has not been seen before," Ferreon said.

"'Formation of this biomolecular condensate is strongly enhanced by a DNA modification called CpG methylation, a change that influences gene expression," said co-corresponding author Dr. Kevin MacKenzie, associate professor of pathology and immunology and of pharmacology and chemical biology at Baylor. "Our results suggest that the local sequence of DNA and its CpG methylation state enable KLF4 to drive DNA into a separate phase, which helps to organize chromatin in three dimensions."

"'Hundreds of human transcription factors contain tandem zinc fingers like those in KLF4, so this class of rapidly evolving proteins may be implicated in chromatin organization through similar 'bridging' interactions," said MacKenzie.

Comment: Expression of instructions from DNA must rely upon DNA 3-D relationships, which means DNA is more than a simple code but designed to have 3-D influences.

Genome complexity: rat mother epigenetics

by David Turell @, Thursday, December 15, 2016, 15:23 (2661 days ago) @ David Turell
edited by David Turell, Thursday, December 15, 2016, 15:37

Rat mothers on a 'western diet' equivalent create kids who end to be fat:

http://www.the-scientist.com/?articles.view/articleNo/47780/title/Study--Rat-Moms--Diet...

"Previous research has suggested a link between a mother’s weight and her offspring’s risk of obesity. But it might have to do more with mom’s diet than her figure, according to a rat study published this month (December 1) in the American Journal of Physiology. Female animals fed a diet with levels of fat, saturated fat, carbohydrates, and protein comparable to a typical Western diet were more likely to give birth to pups at risk for obesity than females fed a lower-fat, higher-grain control diet, even if the moms did not gain weight or struggle to regulate their blood sugar.

"Your diet itself matters, not just whether you are gaining excess weight or developing gestational diabetes,” said coauthor Eric Zorrilla of the Scripps Research Institute, in a press release. This is a key finding that may have implications for managing human pregnancies, added collaborator Jen Frihauf, a PhD student at the University of California, San Diego, while working on the project. “Doctors often use weight gain as a hallmark of a healthy pregnancy,” Frihauf, now a postdoc at Scripps, said in the release. “But we realized there was something going on in utero that wasn’t detectable in the mother’s weight.”

"The increased obesity risk appeared to be lifelong, with offspring more prone to obesity as infants, adolescents, and even adults. The offspring of rats on the Western diet also had altered metabolism, expending less energy while at rest, and elevated levels of insulin, leptin, and adiponectin—a hormone profile that the authors suggest may help detect obesity risk.

"The team also found that offspring of obesity-prone rats that were fed the Western diet were less able to reproduce and more likely to have fewer offspring. “This wasn’t the focus of the study,” Zorilla said in the release. “But it supports the idea that a Western diet promotes infertility in mothers vulnerable to diet-induced obesity.'”

Comment: This epigenetic effect has been seen in many similar circumstances, including the progeny after famine in humans. Changes of this type are metabolic, not species changing. See this on famine:

https://www.sciencedaily.com/releases/2016/12/161212115737.htm

Genome complexity: gene controls

by David Turell @, Friday, December 16, 2016, 01:37 (2661 days ago) @ David Turell

Activation or repression of genes is a tug of war between two processes:

http://medicalxpress.com/news/2016-12-reveals-gene.html

"New research from Stowers Institute for Medical Research suggests the process may be more like a battle between two opposing genetic forces rather than a step-wise assembly of ingredients.

"In their report, published online in Genome Research, Stowers researchers examined regions of fruit fly DNA, called enhancers, which increase the likelihood of gene expression. Gene expression is the process of turning genes on or off, and is crucial for creating specific cells in the body such as nerve cells or cells that make up skin and bone.

"But a duel comes first. Stowers Associate Investigator Julia Zeitlinger, Ph.D., and Postdoctoral Research Associate Nina Koenecke, Ph.D., discovered that DNA enhancers engage in an ongoing contest between activation and repression, which results in a different epigenetic state of the histone proteins around which DNA is wrapped.

"Activation sparks the addition of acetyl groups to histones, which in turn loosen their grip on DNA enhancers, allowing them to be switched on. Repression, on the other hand, removes this acetylation mark and prevents the switch from ever being flipped.

"'Through this balance between forces you can shift an enhancer more easily from inactivity to activity," Zeitlinger says.

***

"The finding therefore clarifies the often misunderstood role of repression in DNA enhancers, and underscores its importance as an action, and not just an inaction. Typically, activation gets the most credit for its role in gene expression. For example, enhancers that are epigenetically modified but still inactive have been thought to be "poised" for future action. However, this new evidence suggests that "poised" enhancers - rather than lacking a key ingredient for activation - may be repressed.

"'When there is an opposition between the two enzymes responsible for acetylation state, it creates an ultra-sensitivity under some conditions," Zeitlinger says. "With just a little more activation, this can create a very dramatic switch in the enhancer's activity. This mechanism could allow a gene being turned on in some cells, while turned off in other cells of the body.'"

Comment: This type of exact knife-edge control is what is needed for precise manufacture of new cells in embryology or replacement cells in adult animals. This mechanism had to be developed at one time since it is a balanced go or no go. It cannot be stepwise or trial and error which is the Darwin approach. It requires precise planning only a mind can bring to the working design

Genome complexity: making specialized cells

by David Turell @, Wednesday, December 21, 2016, 15:17 (2655 days ago) @ David Turell

We start as one cell and make hundreds of different kinds in all our organs. This is how is works:

http://physics.aps.org/articles/v9/147

"How does a liver cell remember that it's a liver cell when it replicates? A cell's identity is determined in part by small molecules that bind to chromosomes at specific locations. Now researchers have devised a model that seems to explain how these so-called epigenetic patterns are sustained across generations of cells. The model connects the epigenetic marking of genes with the three-dimensional structure of DNA as it is folded up inside chromosomes. It leads to a mechanism for patterns of markings to be repaired if they are disturbed by events such as gene replication.

"Epigenetic markings are small molecules added onto parts of chromosomes that may act as genetic switches, silencing some genes and turning on others, so that cells become different types—liver, muscle, or heart cells, for example. Chromosomes are made of chromatin fibers, which are linear DNA molecules looped around cylindrical histone proteins, forming a "string of pearls." A genome’s epigenetic annotations also influence the way that chromatin folds into a three-dimensional shape. This complex folding also affects the activity of genes by preventing the transcription machinery from easily accessing DNA regions that are not at the surface. But the relationships among epigenetic marking, chromatin folding, and gene activity are not completely clear.

***

"There is experimental evidence that in real cells the proteins that write epigenetic marks are recruited by proteins that read the same mark. This protein association can help to sustain epigenetic memory via a positive feedback loop: even if some marks get erased, the presence of others in the same region will encourage the erased marks to be written back again.

***

"The researchers find that an initially random distribution of colors can switch to an ordered state in which the fiber is compactly folded, and the colors are the same over large domains or even the entire chromatin fiber. This change happens abruptly in a so-called first-order phase transition—like water to ice—as long as the bead attraction is strong enough. The ordered state is stable in the presence of occasional disruptions, just as ice will always re-form in the freezer, even if there is some partial melting when someone opens the door. The same basic behavior persists even when the model includes a more realistic description of the kinetics of epigenetic writing.

“'First-order transitions are robust against perturbations,” Michieletto explains, “and so the system has memory.” So even if a large proportion of the epigenetic marks get scrambled, for example, as a cell replicates its genome in preparation to divide, the genome can find its way back to its previous state through a series of rewriting steps. “This aspect is very important for stability and cellular identity,” says Michieletto.

"I really think that this work has great potential,” says Sonja Prohaska, a specialist in epigenetics at the University of Leipzig. “I’m impressed how well the physics and the modeling embed a broad range of observations." She finds the work "astonishingly convincing, and [it] demonstrates that physics has a place in current biology and that it might even simplify a biologist’s life.”

"Mario Nicodemi of the University of Naples in Italy says that it is unclear how the model can be tested by experiments. Michieletto admits that it may take some years before the necessary technology becomes available to make such tests but sees several possibilities. For example, one could manipulate a cell's genes to make it produce non-functional reading or writing proteins, breaking the positive feedback on which the epigenetic memory depends, and compare the effects with the model's predictions.

Comment: this is a physical chemistry attempt to understand how epigenetic markers stay in place as specialized cells reproduce themselves. I think the epigenetic methylation bonds remain strong and corrective measures are very adept at spotting copy errors.

Genome complexity: limiting rogue DNA errors

by David Turell @, Wednesday, December 21, 2016, 15:50 (2655 days ago) @ David Turell

In preparing for reproduction there are mechanisms to prevent the transmission of DNA error segments. The mechanism os also present in somatic tissue:

http://phys.org/news/2016-12-rna-pathway-key-role-health.html

"Humans and other animals carry rogue sequences of DNA in their genomes called transposable elements (TEs). To prevent passing TEs to their offspring, they employ the piRNA pathway in their reproductive organs to block the elements from being active in their sperm and eggs. With a new study in flies, Brown University biologists are the first to show that the anti-TE activity of the piRNA pathway also operates in a normal non-reproductive body tissue, the fly fat body, and that it helps to sustain the life of the animal.

" It's required for normal health and longevity," said Dr. Stephen Helfand, senior author of the study in Nature Communications and a professor of biology at Brown University.

"Most previous reports of piRNA at work outside of reproductive organs were in cancer or stem cells, with one study suggesting it may also be present in a subset of adult fly neurons, but no one had ever measured its consequences in normal health and aging.

"In experiments led by Brown graduate student Brian Jones, the research team tracked several components of the pathway, such as the presence of piRNAs and the expression of associated "piwi" and "flamenco" genes, in the fat body tissue of flies. The fat body is akin to adipose and liver tissues in mammals and also contributes to flies' immune systems.

"Once the researchers confirmed that the piRNA pathway was active in a normal, mature body tissue, they conducted several experiments to see what happened in the flies when they knocked components of the pathway out. For example, with the piwi gene gone, flies had significantly fewer piRNAs than flies who had a copy.

"To see if a compromised pathway led to unchecked transcription of TEs, the researchers used a method that makes cells glow green when particular TEs move around within the genome. Flies without piwi lit up brightly.

"By other measures, the researchers found that piwi-lacking flies experienced increased DNA damage compared to flies with a working piwi gene, and flies lacking in either piwi or flamenco had less fat than controls. Flies without piwi succumbed to starvation more quickly, and flies with either of the genes knocked out lived considerably shorter lives than flies with a working copy of both genes.

"Specifically, about four in five flies with a working piwi gene were still alive at 60 days of age, but virtually all of the piwi-lacking flies were dead long before then. Among flies with a flamenco gene intact, about half were still alive at 60 days, while those lacking any flamenco had died off."

Comment: Reproduction whether it is sexual or simply cellular daughter cell production is vital to life continuing normally. Copy error protection had to be built in from the initiation of life itself. It could not have developed in a stepwise manner as Darwinism assumes.

Genome complexity: telling which cells to develop.

by David Turell @, Friday, December 23, 2016, 21:49 (2653 days ago) @ David Turell

In embryology early generalized cells have to b e told which final type of cell they should. Specific chemical are produced to control this:

http://medicalxpress.com/news/2016-12-embryonic-fate-skin-cells-sweaty.html

"A team of researchers with the Rockefeller University has identified the signals and timing that are involved during embryonic development controlling whether skin cells grow to be sweaty or hairy.

***

"Mice are unique because they have skin cells on their backs that only allow for the development of hair follicles and skin cells on their feet that only allow for the development of sweat glands. This allowed the researchers an opportunity to learn more about such development by comparing the two. They found that stem cells that led to skin development in mice had differences in RNA expression of proteins that were involved in controlling which type of cell structure would develop—one type, called mesenchymal-derived bone morphogenetic proteins, were, for example, more plentiful in cells found in the feet—one in particular, Bmp5, was found to play a particularly important role. When it was blocked, the number of sweat glands that developed in mice feet was greatly reduced. The team also found other mechanisms involved, such as WNT and FGF proteins, which, when switched in mice, resulted in cells developing swapped end results, e.g. hair follicles instead of sweat glands.

"The team compared these results with human skin cell samples and found that BMP and FGF proteins were expressed at higher levels during week 17 of fetal development than during week 15, which prior research has shown is a period when skin cell progression moves from hair to sweat-bud formation."

Comment: Note the complexity here. In the development of the embryo, timing is everything so parts form in proper sequence and relationship to all other parts. Chemical signals must appear on time to create the proper cells in the proper place. Cells become either hair or sweat glands, but there are also oil glands not mentioned in this article. All start from the same progenitor cell. How the chemicals listed in the article teach the DNA in each cell to differentiate the cell into the exact type needed is currently unknown. There is also the issue of proper placement of oil and sweat glands and the hair follicles. And evolution developed all of this process by chance. No way! This biology alone negates Darwin's thoughts about evolution. His only contribution is the concept of evolution by common descent, nothing of the methodology of how it happened.

Genome complexity: epigenetically handling poisons

by David Turell @, Thursday, February 23, 2017, 21:22 (2591 days ago) @ David Turell

Natives in the Chili can handle arsenic in their diets:

https://www.newscientist.com/article/mg23331144-200-desert-people-evolve-to-drink-water...

"For settlers in the Quebrada Camarones region of Chile’s Atacama desert some 7000 years ago, water posed more than a bit of a problem. They were living in the world’s driest non-polar desert, and several of their most readily available water sources, such as rivers and wells, had high levels of arsenic, which can cause a variety of health problems.

"The arsenic contamination here exceeds 1 microgram per litre: the highest levels in the Americas, and over 100 times the World Health Organization’s safe limits. There are virtually no alternative water sources, and yet, somehow, people have survived in the area. Could it be that arsenic’s negative effects on human health, such as inducing miscarriages, acted as a natural selection pressure that made this population evolve adaptations to it? A new study suggests this is indeed so.

"The body uses an enzyme called AS3MT to incorporate arsenic in two compounds, monomethylarsonic (MMA) acid and dimethylarsinic (DMA) acid. People who metabolise arsenic more efficiently convert more of it into the less toxic, more easily expelled DMA.

"Mario Apata of the University of Chile in Santiago and his colleagues looked at variations in the gene coding for AS3MT in nearly 150 people from three regions of the country. They found higher frequencies of the protective variants in people from Camarones: 68 per cent there had them, as opposed to just 48 and 8 per cent of people in the other two. “Our data suggest that a high arsenic metabolization capacity has been selected as an adaptive mechanism in these populations in order to survive in an arsenic-laden environment,” the researchers conclude (American Journal of Physical Anthropology, doi.org/bz4s).

"The variants that protect the Camarones people are called single nucleotide polymorphisms – changes in a single DNA letter of the genetic code. Anthropologist Lorena Madrigal of the University of South Florida in Tampa says these are such tiny mutations that they aren’t telling us exactly how the changes affect the enzyme molecule and its detoxifying effects.

"Previous studies found similar mutations in the AS3MT gene that contribute to improved arsenic metabolisation in Vietnam and Argentina. Sequencing the entire chromosomal region around this gene could reveal more, but there’s still a long way to go before we fully understand the molecular mechanism for how arsenic resistance works.

***

"Another notable example of recent human evolution is lactose tolerance. A mutation which allowed adults to keep producing the enzyme lactase to digest milk emerged around 7000 years ago, alongside dairy farming, and now 35 per cent of adults carry it and can digest milk as a result."

Comment: The soil in Chili is polluted by all the volcanism in the Andes. Llamas can tolerate and need enormous amounts of Selenium that would otherwise kill. the body is built to adapt to poisonous situations God could not prevent.

Genome complexity: Electrons aid in DNA replication

by David Turell @, Monday, February 27, 2017, 01:32 (2588 days ago) @ David Turell

Electrons running along DNA for repair and to speed replication:

https://phys.org/news/2017-02-electrons-dna-wire-replication.html

"The electron transfer process in DNA occurs very quickly," says O'Brien, lead author of the study, appearing in the February 24 issue of Science. "It makes sense that the cell would utilize this quick-acting pathway to regulate DNA replication, which necessarily is a very rapid process."

"The researchers found their first clue that DNA replication might involve the transport of electrons through the double helix by taking a closer look at the proteins involved. Two of the main players in DNA replication, critical at the start of the process, are the proteins DNA primase and DNA polymerase alpha. DNA primase typically binds to single-stranded, uncoiled DNA to begin the replication process. It creates a "primer" made of RNA to help DNA polymerase alpha start its job of copying the single strand of DNA to create a new segment of double-helical DNA.

***

"DNA primase and DNA polymerase alpha molecules both contain iron-sulfur clusters. Barton and her colleagues previously discovered that these metal clusters are crucial for DNA electron transport in DNA repair. In DNA repair, specific proteins send electrons down the double helix to other DNA-bound repair proteins as a way to "test the line," so to speak, and make sure there are no mutations in the DNA. If there are mutations, the line is essentially broken, alerting the cell that mutations are in need of repair. The iron-sulfur clusters in the DNA repair proteins are responsible for donating and accepting traveling electrons.

***

"Through a series of tests in which mutations were introduced into the DNA primase protein, the researchers showed that this protein needs to be in an oxidized state—which means it has lost electrons—to bind tightly to DNA and participate in DNA electron transport. When the protein is reduced—meaning it has gained electrons—it does not bind tightly to DNA.

"'The electronic state of the iron-sulfur cluster in DNA primase acts like an on/off switch to initiate DNA replication," says O'Brien.

"What's more, the researchers demonstrated that electron transport through DNA plays a role in signaling DNA primase to leave the DNA strand. (Though DNA primase must bind to single-stranded DNA to kick off replication, the process cannot begin in earnest until the protein pops back off the strand).

"The scientists propose that the DNA polymerase alpha protein, which sits on the double helix strand, sends electrons down the strand to DNA primase. DNA primase accepts the electrons, becomes reduced, and lets go of the DNA. This donation and acceptance of electrons is done with the help of the iron-sulfur clusters.

"'You have to get the DNA primase off the DNA quickly—that really starts the whole replication process," says Barton. "It's a hand off of electrons from one cluster to the other through the DNA double helix."

"Many proteins involved in DNA reactions also contain iron-sulfur clusters and may also play roles in DNA electron transport chemistry, Barton says."

Comment: Can the workings of the genome get more complex that is now known. Absolutely. We've just begun to see how complex it is. Not by chance!

Genome complexity: new epigenetic marks

by David Turell @, Tuesday, February 28, 2017, 18:07 (2586 days ago) @ David Turell

Not just methylation but now M1A and M6A and others are found but exact function not clear:

http://www.nature.com/nature/journal/v542/n7642/full/542503a.html

"at least one-quarter of our mRNAs harbour chemical tags — decorations to the A, C, G and U nucleotides — that are invisible to today's sequencing technologies. (Similar chemical tags, called epigenetic markers, are also found on DNA.) Researchers aren't sure what these chemical changes in RNA do, but they're trying to find out.

"A wave of studies over the past five years — many of which focus on a specific RNA mark called N6-methyladenosine (m6A) — have mapped these alterations across transcriptomes and demonstrated their importance to health and disease. But the problem is vast: these marks coat not only mRNA but other RNA transcripts as well, and they cut across all the domains of life and beyond, marking even viruses with their presence.

"The modifications themselves are not new. What has given them meaning and driven epitranscriptomics into the spotlight is the discovery of enzymes that can add, remove and interpret them. In 2010, chemical biologist Chuan He at the University of Chicago, Illinois, proposed that these chemical tags could be reversible and important regulators of gene expression. Not long afterwards, his group demonstrated2 the first eraser of these marks on mRNA, an enzyme called FTO. That discovery meant that m6A wasn't just a passive mark — cells actively controlled it. And this realization came at about the same time that global approaches, harnessing the power of next-generation sequencing, made it possible to map m6A and other modifications across the transcriptome.

***

"Other RNA modifications have also attracted researchers' attention. In 2016, teams led by chemist Chengqi Yi at Peking University in Beijing and by Rechavi and He used antibody-based methods to map N1-methyladenosine (m1A) in mouse and human cell lines and tissues8. Using different approaches to prevent m1A from interfering with reverse transcription, the two teams showed that m1A, which was discovered in total RNA in the early 1960s, is present on mRNA at the position at which the translation machinery initiates protein production. Stress conditions alter the maps, suggesting that they are dynamic.

"The researchers don't yet know what m1A does, but they have a tantalizing clue: most transcripts have only one m1A site, and these seem to be translated more often than those that lack the modification. “This is very exciting — and of course challenging — because we are dealing with a new regulatory mechanism for translation of messenger RNA,” Rechavi says. An antibody that targets m1A is available from MBL International.

***

"Technical hurdles remain, however, as RNA poses challenges not seen in DNA. One is that RNA readily folds in on itself to form loops and knots, so it is highly structured. In its study15, Oxford Nanopore attached RNA to cDNA, which helps 'iron out' the secondary structures and move the RNA through the pore. A second challenge is that RNA degrades more easily than DNA, a problem that may stymie long-read sequencing approaches.

"Yet another challenge, on the data side, is the sheer number of RNA modifications. Recognition of multiple different modifications on the same RNA would require massive training sets to teach the detection software to distinguish one modification from another. Winston Timp, a biomedical engineer at Johns Hopkins University in Baltimore, Maryland, has been using Oxford Nanopore technology to develop new methods for detecting specific DNA modifications. He now plans to move into RNA modifications, developing a training set that will help recognize m6A modifications. “The problem is, we don't know how diverse on a given molecule the modifications are,” he says. “But this is something we can probe. It's an exciting area of research.'”

Comment: We are seeing only the tip of the research iceberg. How much complexity is needed before it is recognized a designer, God, did this.

Genome complexity: plant sugar vs, oil production

by David Turell @, Sunday, March 19, 2017, 23:24 (2567 days ago) @ David Turell

Plants make sugars easily with photosynthesis, but they can also make oils which is much more energy intensive. To do that sugar production is turned off using phosphorylation marks:

https://www.sciencedaily.com/releases/2017/03/170317152721.htm

"Even plants have to live on an energy budget. While they're known for converting solar energy into chemical energy in the form of sugars, plants have sophisticated biochemical mechanisms for regulating how they spend that energy. Making oils costs a lot.

***

"When sugar is low, this protein, known as KIN10, adds a phosphate group to as many as a thousand different proteins to change their functions in ways that ultimately increase sugar levels, Shanklin explained. As sugar levels increase KIN10's ability to phosphorylate proteins becomes inhibited, slowing down sugar production.

***

"This protein, known as WRINKLED1, turns on the genes that make oil," Shanklin said.

***

"To investigate the connection further, the team purified these proteins (KIN10 and WRINKLED1) and used a radioactive form of the element phosphorus to trace the phosphorylation reaction.

***

"'When sugar is low, KIN10 phosphorylates WRINKLED1, marking it for destruction, so less WRINKLED1 is available to turn on oil production," Shanklin said. "Conversely, when sugar levels rise -- when times are good -- KIN10 is turned off and WRINKLED1 levels go up and drive oil production."

"The details of the study offer several possible ways for scientists to modify WRINKLED1 to try to "trick" plants into making more oil: One is to alter the sites that get phosphorylated; the other is to interfere with sites that enable the phosphorylated protein to enter the recycling machinery.

"'Nature makes genetic 'on-switches' short lived to enable rapid responses to changing metabolic conditions," said Shanklin. "So we don't need to make more of the oil-production 'on-switch,' we just need to prevent the protein from being degraded so it accumulates and we get stronger effects.'"

Comment: Plants show as much genome complexity as animals. Hard to imagine this developed stepwise.

Genome complexity: early steps reproducing DNA

by David Turell @, Sunday, March 19, 2017, 23:38 (2567 days ago) @ David Turell

As usual very complex right formation:

https://phys.org/news/2017-03-human-dna-replication-captured-atomic.html

"The process is so complex, calling for the orchestration of over a hundred highly specialized proteins, each of which must play its part at precisely the right moment and in the proper spatial orientation. It has often been compared to an exquisitely choreographed molecular dance. The smallest errors, left uncorrected, can have deadly consequences

***

"The images of the human version of this complex, called ORC - for origin recognition complex - show it in its active mode.

"ORC complexes self-assemble in the cell nucleus and bind at specific spots called start sites or origins along the double helix in chromosomes. In human cells, ORC assembles at literally thousands of origin sites across the entire genome, to form an initial configuration called the pre-replication complex, or pre-RC. Once assembled, these pre-RCs are like highly prepared Olympic swimmers standing on the starting block, waiting for the signal to start the race.

"Like fast swimmers, each complex needs fuel to recruit its "motor" that opens the two strands of the double helix. In the case of ORC it is ATP, or adenosine triphosphate. In ORC's active phase, the researchers showed that a subassembly containing ORC subunits 1,2,3,4 and 5 engages multiple ATP molecules and forms a partial ring-shaped complex. ATP is also used to recruit another protein component called CDC6, transforming the open ring into a closed ring. By this time, the multi-part assembly has engaged and bound to the double helix, which passes through the center of the ring like a bolt through the center of a nut. The ring is designed to fit the DNA snugly.

***

"Although ORC in primitive yeast and complex human beings operates differently - the yeast protein is stable during cell division while in humans it is dynamically assembled and taken apart - they are "remarkably similar" in important respects, the researchers note.

"'Both are highly similar to another ATP-driven machine that also loads a ring-shaped protein onto DNA, the DNA polymerase clamp-loaders, showing that these molecular machines that load ring-shaped proteins onto DNA have been re-purposed for multiple stages of DNA replication," the team writes. They both act as molecular switches that hydrolyze the energy of ATP to lock protein rings on double strand DNA. "

Comment: More understanding of the complexity involved. There is no way to develop this process stepwise without inviting fatal errors. Only saltation fits originating this process.

Genome complexity: more RNA complexity

by David Turell @, Sunday, March 26, 2017, 21:51 (2560 days ago) @ David Turell

The epigenetic changes in RNA has multiple controls a new paper discusses:

https://www.sciencedaily.com/releases/2017/03/170322103721.htm

In epigenetics, there there are "accents," called DNA methylation, which means having a C or a methyl-C. The first one usually means that a gene is expressed and active, while the second one implies that a gene is silent and inactive. Our DNA "speaks" when it produces another molecule called RNA (Ribonucleic Acid). Until very recently, it was believed that this molecule was only a poorly regulated intermediate capable of producing proteins (such as insulin, hemoglobin and others) under DNA's orders.

"Today, an article published in Cancer Discovery by Manel Esteller, Director of the Epigenetics and Cancer Biology Program of Bellvitge Biomedical Research Institute (IDIBELL), ICREA Researcher and Professor of Genetics at the University of Barcelona, explains that this RNA also has its own spelling and grammar, just like DNA. These "epigenetics of RNA" are called epitranscriptome.

"It is well-known that sometimes DNA produces a RNA string but then this RNA does not originate the protein. Because in these cases the alteration is neither in the genome nor the proteome, we thought it should be in the transcriptome, that is, in the RNA molecule," Dr. Esteller explains."In recent years, we discovered that our RNA is highly regulated and if only two or three modifications at the DNA level can control it, there may be hundreds of small changes in RNA that control its stability, its intracellular localization or its maturation in living beings."

"In human cells, this field did not start to be studied in depth in the last five years. "For example, we now know that RNA can be methylated just like DNA and in a highly specific way," says Dr. Manel Esteller, "and even more recently we observed that these epigenetic modifications of RNA may be key in the regulation of "guardian" RNAs, also called non-coding RNAs."

"The article also points out that the epitranscriptome could be altered in some human diseases, while alterations in genes responsible for cancer are also being discovered. "It will definitely be an exciting research stage for this and the next generation of scientists," concludes the researcher."

Comment: the layers of genetic control just get deeper and deeper. Not by chance!

Genome complexity: DNA repair

by David Turell @, Sunday, March 26, 2017, 22:08 (2560 days ago) @ David Turell

Another complex interaction of molecules to repair damaged DNA:

https://phys.org/news/2017-03-scientists-critical-dna-cellular-aging.html


"The findings, to be published March 24 in Science, offer a critical insight into how and why the body's ability to fix DNA dwindles over time and point to a previously unknown role for the signaling molecule NAD as a key regulator of protein-to-protein interactions in DNA repair. NAD, identified a century ago, is already known for its role as a controller of cell-damaging oxidation.

"Additionally, experiments conducted in mice show that treatment with the NAD precursor NMN mitigates age-related DNA damage and wards off DNA damage from radiation exposure.

***


"The researchers already knew that NAD, which declines steadily with age, boosts the activity of the SIRT1 protein, which delays aging and extends life in yeast, flies, and mice. Both SIRT1 and PARP1, a protein known to control DNA repair, consume NAD in their work.


"Another protein, DBC1, one of the most abundant proteins in humans and found across life forms from bacteria to plants and animals, was a far murkier presence. Because DBC1 previously had been shown to inhibit vitality-boosting SIRT1, the researchers suspected DBC1 may also somehow interact with PARP1, given the similar roles PARP1 and SIRT1 play.

"'We thought if there is a connection between SIRT1 and DBC1, on one hand, and between SIRT1 and PARP1 on the other, then maybe PARP1 and DBC1 were also engaged in some sort of intracellular game," said Jun Li, first author on the study and a research fellow in the Department of Genetics at HMS.


"To get a better sense of the chemical relationship among the three proteins, the scientists measured the molecular markers of protein-to-protein interaction inside human kidney cells. DBC1 and PARP1 bound powerfully to each other. However, when NAD levels increased, that bond was disrupted. The more NAD was present inside cells, the fewer molecular bonds PARP1 and DBC1 could form. When researchers inhibited NAD, the number of PARP1-DBC1 bonds went up. In other words, when NAD is plentiful, it prevents DBC1 from binding to PARP1 and meddling with its ability to mend damaged DNA.


"What this suggests, the researchers said, is that as NAD declines with age, fewer and fewer NAD molecules are around to stop the harmful interaction between DBC1 and PARP1. The result: DNA breaks go unrepaired and, as these breaks accumulate over time, precipitate cell damage, cell mutations, cell death, and loss of organ function.


"Next, to understand how exactly NAD prevents DBC1 from binding to PARP1, the team homed in on a region of DBC1 known as NHD, a pocket-like structure found in some 80,000 proteins across life forms and species whose function has eluded scientists. The team's experiments showed that NHD is an NAD binding site and that in DBC1, NAD blocks this specific region to prevent DBC1 from locking in with PARP1 and interfering with DNA repair.


"Sinclair said that since NHD is so common across species, the finding suggests that by binding to it, NAD may play a similar role averting harmful protein interactions across many species to control DNA repair and other cell survival processes.


"To determine how the proteins interacted beyond the lab dish and in living organisms, the researchers treated young and old mice with the NAD precursor NMN, which makes up half of an NAD molecule. NAD is too large to cross the cell membrane, but NMN can slip across it easily. Once inside the cell, NMN binds to another NMN molecule to form NAD.

"As expected, old mice had lower levels of NAD in their livers, lower levels of PARP1, and a greater number of PARP1 with DBC1 stuck to their backs.

"After receiving NMN with their drinking water for a week, however, old mice showed marked differences both in NAD levels and PARP1 activity. NAD levels in the livers of old mice shot up to levels similar to those seen in younger mice. The cells of mice treated with NMN also showed increased PARP1 activity and fewer PARP1 and DBC1 molecules binding together. The animals also showed a decline in molecular markers that signal DNA damage.

"In a final step, scientists exposed mice to DNA-damaging radiation. Cells of animals pre-treated with NMN showed lower levels of DNA damage. Such mice also didn't exhibit the typical radiation-induced aberrations in blood counts, such as altered white cell counts and changes in lymphocyte and hemoglobin levels. The protective effect was seen even in mice treated with NMN after radiation exposure.

"Taken together, the results shed light on the mechanism behind cellular demise induced by DNA damage. They also suggest that restoring NAD levels by NMN treatment should be explored further as a possible therapy to avert the unwanted side effects of environmental radiation, as well as radiation exposure from cancer treatments."

Comment: Ever increasing complexity. DNA must b e protected or life stops. Not by chance!

Genome complexity: stem cell controls

by David Turell @, Tuesday, March 28, 2017, 23:19 (2558 days ago) @ David Turell

This molecular system controls the expression of pluripotent stem cells into a more specialized state:

"Bioengineers at the University of California San Diego have discovered a protein that regulates the switch of embryonic stem cells from the least developed "naïve" state to the more developed "primed" state. This discovery sheds light on stem cell development at a molecular level.

***

"'A number of previously identified regulatory proteins can be considered as rough-tuning knobs that result in greater changes in cellular behavior. We need both tools to precisely set stem cells into the desired cellular state so that they can carry out the functions that we desire."

"The researchers discovered that the protein, called SMARCAD1, interacts with a specific type of histone modification, called histone citrullination (H3R26Cit), to prevent the spontaneous switch from the naïve to the primed pluripotent state. By suppressing SMARCAD1 from interacting with H3R26Cit, researchers were able to induce this switch. They also found that the stem cells with suppressed SMARCAD1 expression remained pluripotent. "This finding offers an approach to fine tune the stem cells between two cellular states corresponding to two early developmental stages," said Jia Lu, a bioinformatics Ph.D. student in Zhong's research group who co-authored this work.

"Zhong and his team first used protein arrays composed of hundreds of histone peptides harboring distinct post-transcriptional modifications, and found that SMARCAD1 specifically interacts with the H3R26Cit modification. They then used a technology called ChIP-seq to assay genome-wide distributions of SMARCAD1 binding as well different kinds of histone modifications, and found that SMARCAD1 specifically binds to H3R26Cit modified histones in the entire genome.

"Researchers also conducted experiments in which they suppressed the expression of SMARCAD1, and a separate set of experiments in which they suppressed a more general form of H3R26Cit called H3Cit. In both experiments, they observed cellular changes consistent with the switch from the naïve to the primed stem cell state, providing more evidence of SMARCAD1's regulatory role in stem cell development."

Comment: Systems like this have feedback loops to control toe exact level of the stem cells activity. That is yet to be found. More and more complexity of the genome. not by chance!

Genome complexity: DNA repair

by David Turell @, Tuesday, July 18, 2017, 15:40 (2446 days ago) @ David Turell

Another study showing cell DNA repair by two methods:

https://www.sciencedaily.com/releases/2017/07/170712074220.htm

"Japanese researchers from Osaka University have uncovered a way in which our cells regulate the repair of broken DNA. Their results, published in the journal "Cell Reports," show a common molecule regulates multiple repair mechanisms and help shed light on how the cell maintains the integrity of the human genome when it is damaged

***

"'The two mechanisms in the cell are non-homologous end joining (NHEJ) and homologous recombination (HR) for repairing DNA double strand break" explains Chikashi Obuse, Professor at the Osaka University Graduate School of Sciences.

"While NHEJ and HR both function to repair damaged DNA, they respond to different situations; types of damage, presence or absence of homologous template or cell cycle stages etc. What has continued to elude researchers is how the cell knows which system to call. Obuse shows in his latest report that the protein suppressor of cancer cell invasion (SCAI) plays an important role for the selection of HR.

"To study the function of SCAI, Obuse and his team of scientists exposed human cells to X-ray irradiation to damage the DNA.

"'Our results suggested SCAI bound to 53BP1 to promote the recruitment of HR proteins. When we depleted SCAI these proteins did not accumulate," he said.

"In particular, Obuse highlighted the great diminishment of the protein BRCA1 at damage sites when SCAI was depleted. On the other hand, SCAI presence inhibited another protein, RIF1, to promote the recruitment of BRCA1.

"'RIF1 is known to inhibit BRCA1 accumulation at DNA damaged sites. It binds to 53BP1. When we looked at confocal imaging of cells, we saw RIF1 initially accumulated at sites of DNA damage but was gradually replaced by SCAI," said Obuse.

"This led the scientists to wonder if SCAI and RIF1 competed to bind to 53BP1 and whether this binding determined the DNA repair mechanism.

"Indeed, additional experiments showed that the phosphorylation state of 53BP1 determined its binding partner.

"'The next question for us is to determine which upstream kinases are responsible for phosphorylating the sites of 53BP1 needed for binding with SCAI," added Obuse. "The upstream signaling molecules will be important for helping to determine the cell's choice for either the NHEJ or HR pathway.'"

Comment: Since DNA is vital and can be damaged, a repair mechanism had to be in place when DNA first appeared. Enzymes are involved. This could not have developed stepwise, but all at once. Another saltation by God.

Genome complexity: epigenetic eye loss?

by David Turell @, Thursday, October 12, 2017, 18:28 (2360 days ago) @ David Turell

Blind cave fish lost their eyes. The mechanism is debated in a new study:

https://www.newscientist.com/article/2150233-did-blind-cavefish-evolve-by-breaking-the-...

"Over the past few million years, blind forms of the Mexican tetra (Astyanax mexicanus) have evolved in caves. Maintaining eyes and the visual parts of the brain uses lots of energy, so the loss of eyes is a big advantage for animals living in the dark. Instead the cavefish “see” by sucking.

"It was assumed that these fish became blind because mutations disabled key genes involved in eye development. This has been shown to be the case for some other underground species that have lost their eyes.

"But Aniket Gore of the US’s National Institute of Child Health and Human Development and colleagues haven’t found any disabling changes in the DNA sequences of eye development genes in the cavefish.

"Instead, the genes have been switched off by the addition of chemical tags called methyl groups. This is what is known as an epigenetic, rather than genetic, change.

“'Although a central role for DNA methylation in development and disease has been well-documented, our results suggest that epigenetic processes can play an equally important role in adaptive evolution,” the team writes.

"The researchers propose that this epigenetic mechanism allowed the cavefish to shed its eyes faster than if the change had happened via DNA mutations in eye genes.

"That is a controversial suggestion, and one that will be music to the ears of those who think that evolution can occur via heritable epigenetic mechanisms, and that standard evolutionary theory needs to be broadened to include such processes.

“'This is a most interesting paper,” says evolutionary biologist Douglas Futuyma of Stony Brook University in New York. But he doesn’t think it poses any challenge to standard evolutionary theory as the epigenetic change is itself most likely a result of a genetic change.

"Gore’s team shows that the silencing of the eye genes is due to the increased activity of a specific gene involved in methylation, Futuyma points out. So the question then is, what is making this gene more active?

“'I think it likely that there has been an alteration in DNA sequence of that gene,” he says.

“'You cannot completely rule out genetic mutations,” says Eva Jablonka of Tel Aviv University, Israel, who thinks evolution can occur via epigenetic changes and that we need a new evolutionary synthesis. “Maybe there was genetic variation that contributed to the eye loss.”

"However, Jablonka thinks that heritable epigenetic changes alone could explain the loss of eyes. What is more, she even thinks it possible that the epigenetic changes were somehow triggered by the cave environment in the first place. That would be a form of Lamarckian evolution: the idea that characteristics acquired during an individual’s lifetime can be passed on to descendants.

"David Shuker at the University of Edinburgh, UK, is unconvinced by this or any of the other proposed examples of evolution via epigenetic mechanisms.

"There is no doubt that some animals respond to the environment via epigenetic mechanisms, he says, but these mechanisms have evolved via genetic changes. “It goes through genetically built systems,” Shuker says.

"So, like Futuyma, he thinks standard evolutionary processes such as mutation and natural selection still explain all we have discovered.

“'We are always finding new ways in which these processes manifest themselves,” says Shuker. “We have found lots of amazing things.” But the basic principles remain valid, he says.

"Shuker is suspicious of some efforts to promote the idea of an “extended evolutionary synthesis”. He thinks some people are trying sneak religious ideas back into evolutionary theory. (my bold)

“They are trying to allow organisms to have agency not controlled by genes,” he says.

Comment: Once again we see the battle between atheistic Neo-Darwin defenders and those who champion epigenetics as a definitive adaptive mechanism that might represent religious ideas. This applies directly to our discussion about Darwinists and atheism. Random mutation and natural selection for them obviously denies God.

Genome complexity: video 3-D DNA dance

by David Turell @, Friday, October 13, 2017, 15:01 (2359 days ago) @ David Turell

Video: https://youtu.be/Q_KdrtsmYoE

Not by chance!

Genome complexity: complex telomere structure

by David Turell @, Wednesday, April 25, 2018, 20:44 (2165 days ago) @ David Turell

An unbelievably complex enzyme protein complex makes the telomere:

https://www.nature.com/articles/d41586-018-04756-3?utm_source=breakingnews&utm_medi...

"In a paper published in Nature, Nguyen et al.4 report a structure of human telomerase bound to DNA, providing an unprecedented view of how the enzyme complex is organized and establishing a framework for drug discovery.

"Telomerase is a ribonucleoprotein (RNP) enzyme — part RNA, part protein. To retain normal function, the enzyme must contain at least a telomerase reverse transcriptase (TERT) protein subunit and a long, non-coding telomerase RNA (TR). Telomerase complexes also usually include several species-specific proteins that are important for regulating RNP assembly5. The enzyme maintains telomeres by catalysing the addition of simple DNA-sequence repeats onto the ends of linear chromosomes. The catalytic TERT subunit uses a small portion of TR as a template for these repeats.

"Vertebrate telomerases also belong to the family of box H/ACA RNP complexes, which generally modify essential cellular RNAs such as transfer RNAs, ribosomal RNA and spliceosomal RNA6. Curiously, despite possessing the RNA and protein components of H/ACA RNPs, telomerase does not exhibit the RNA-modifying activity typically associated with this class of complex.

***

"The structural segregation of the catalytic core and H/ACA lobe raises the question of why the telomerase complex has retained the large H/ACA RNP throughout evolution. Part of the answer is likely to be that TCAB1 is needed to mediate trafficking of telomerase components during RNP assembly. However, another striking feature of the H/ACA lobe is that its proteins seem to promote a specific conformation of TR that brings the CR4/5 domain close to the catalytic core, where it is needed to support catalysis. This bears a remarkable resemblance to the T. thermophila telomerase RNP, in which an RNA-binding protein called p65 is required to remodel TR and promote contacts with the catalytic TERT subunit13,17. This resemblance suggests that telomerases from different organisms have co-opted different types of RNA-binding protein to promote RNP assembly. The idea that the H/ACA proteins direct RNA folding can be tested experimentally, using the new structural model as a framework with which to design and interpret incisive experiments.

"Nguyen and colleagues’ work sets a new bar for structural models of human telomerase, but there is still work to be done. A complete view of telomerase structure and function will require atomic-resolution models of the enzyme in its various functional states. Advances in cryoEM techniques, together with other structural and biophysical tools, will no doubt continue to enhance our appreciation of the intricate workings of this fascinating enzyme."

Comment: Be sure to look at the illustration of this structure. This is a giant molecule enzyme which protects chromosomes all during life as cells divide constantly. It is a vital part of living material. Not found by any chance mechanism. Must have been designed.

Genome complexity: starts with a single fertilized egg

by David Turell @, Friday, April 27, 2018, 01:55 (2164 days ago) @ David Turell

We are starting to follow and ledarn the development of an embryo by studying how individual cells from the first division onward progress to become aggregates of different organ cells:

https://phys.org/news/2018-04-scientists-reveal-genetic-roadmap-entire.html

"From this solitary cell emerges the galaxy of others needed to build an organism, with each new cell developing in the right place at the right time to carry out a precise function in coordination with its neighbors.

"This feat is one of the most remarkable in the natural world, and despite decades of study, a complete understanding of the process has eluded biologists.

***

"Using single-cell sequencing technology, the research teams traced the fates of individual cells over the first 24 hours of the life of an embryo. Their analyses reveal the comprehensive landscape of which genes are switched on or off, and when, as embryonic cells transition into new cell states and types.

"Together, the findings represent a catalog of genetic "recipes" for generating different cell types in two important model species and provide an unprecedented resource for the study of developmental biology and disease.

***

"'Understanding how an organism is made requires knowing which genes are turned on or off as cells make fate decisions, not just the static sequence of a genome," Megason said. "This is the first technological approach that has allowed us to systematically and quantitatively address this question."

***

"In both species, the teams' findings mirrored much of what was previously known about the progression of embryonic development, a result that underscored the power of the new approaches. But the analyses were unprecedented in revealing in comprehensive detail the cascades of events that take cells from early progenitor or "generalist" states to more specialized states with narrowly defined functions.

"The teams identified otherwise difficult-to-detect details such as rare cell types and subtypes and linked new and highly specific gene expression patterns to different cell lineages. In several cases, they found cell types emerging far earlier than was previously thought.

***

"When Klein, Kirschner, Megason and colleagues compared cell-state landscapes between zebrafish and frog embryos, they observed mostly similarities. But their analyses revealed numerous surprises as well. One such observation was that genes marking cell states in one species were often poor gene markers for the same cell state in the other species.In several instances, they found that the DNA sequence of a gene—and the structure of the protein it encodes—could be nearly identical between species but have very different expression patterns.

"'This really shocked us, because it goes against all the intuition we had about development and biology," Klein said. "It was a really uncomfortable observation. It directly challenges our idea of what it means to be a certain 'cell type.'"

***

"In another striking finding, the teams observed that the process of cell differentiation into distinct cell types—which is commonly thought to occur in a tree-like structure where different cell types branch off from a common ancestor cell—can form "loops" as well as branches.

"For example, the neural crest—a group of cells that give rise to diverse tissue types including smooth muscle, certain neurons and craniofacial bone—initially emerges from neural and skin precursors, but is well-known to generate cells that appear almost identical to bone and cartilage precursors.

"The new results suggest that similar loops might occur in other situations. That cells in the same state can have very different developmental histories suggests that our hierarchical view of development as a "tree" is far too simplified, Klein said.

"All three teams also identified certain cell populations that existed in a kind of intermediate "decision making" state. Schier and colleagues found that, at certain key developmental branch points, cells appeared to go down one developmental trajectory but then changed their fate to another trajectory.

"Klein, Megason, Kirschner and colleagues made a related observation that, early in development, some cells activated two distinct developmental programs. Though those intermediate cells would eventually adopt a single identity, these discoveries add to the picture of how cells develop their eventual fate and hint that there may be factors beyond genes involved in directing cell fate.

"'With multilineage cells, we have to start wondering if their final fate is being determined by some selective force or interaction with the environment, rather than just genetic programs," Kirschner said."

Comment: Darwin ignored embryology, and there is no answer for it in his theory. Note how complex the problem is to understand, and recognize that a fertilized egg, one cell, makes the whole individual. Not by chance. To me this is the equivalent of trying to explain consciousness. A whole human in nine months!

Genome complexity: we survive constant mutations

by David Turell @, Friday, May 11, 2018, 22:00 (2149 days ago) @ David Turell

This article describes the multitude of mutations that occur during a lifetime, generally without harm:

https://www.theatlantic.com/science/archive/2018/05/your-body-acquires-trillions-of-new...

"As you read this article, the cells in your body are dividing and the DNA in them is being copied, letter by letter. So long is the human genome—more than 3 billion letters—that even an astonishingly low error rate of one in many million letters could amount to 10 new mutations every time a cell divides.

"Oh, perhaps you’re also catching some sun (ultraviolet rays) while you read this, or enjoying a beer (alcohol), or have recently been high in the atmosphere on an airplane (cosmic rays). Congratulations, you’ve given yourself even more mutations. In a typical day, scientists estimate, the 37 trillion cells in your body will accumulate trillions of new mutations.

***

“'It sounds very scary,” acknowledges Cristian Tomasetti, a cancer researcher at Johns Hopkins. “Fortunately for us,” he says, “the great majority of places where these mutations may hit don’t have important consequences.”

***

"A small number of those mutations could strike in a cancer gene, making individual cells better at dividing and growing. But one mutation isn’t usually enough to make the cell cancerous. “Evolution has built in a formidable number of safety nets,” says Jan Vijg, a geneticist at the Albert Einstein College of Medicine. For example, a cancer cell needs to override the natural limit on how many times a cell can divide. It needs to escape “apoptosis,” or the cell’s tendency to self-destruct when something goes wrong. And it needs to evade an immune system that is constantly on the lookout for aberrant cells. A single cell must accumulate all these mutations to be become successfully cancerous.

"Not all cells in the body accumulate mutations equally. A lot of this has to do with simply how frequently these cells divide. You’re constantly shedding the lining of your gut, for example, so those cells need to divide frequently to replace others.

" Tomasetti says, lung cells may come into frequent contact with tobacco smoke or pollution, which can cause mutations in their own right. Skin, on the other hand, is frequently exposed to sunlight. In one study, eyelid skin on middle-aged and elderly people—who have been through decades of sun exposure—had a stunningly high number of mutations: 60 to 180 in the genes of each cell.


"Vijg has also compared the mutation rate in germ-line cells (sperm and eggs) with somatic cells (everything else, including your skin, liver, blood, etc.). Only the mutations in germ-line cells can get passed on to your children. And germ-line cells appear to have some way of suppressing mutations, perhaps through more robust DNA repair. The cells that make sperm, for example, are constantly dividing to make more sperm, but the mutation rate in sperm is less than one-tenth of that somatic cells.

"Once sperm meets egg, the fertilized egg begins to divide. And once it begins to divide, it begins making mistakes in DNA replication. “Even from the minute we’re conceived, our cells are accumulating mutations,” says Peter Campbell, a cancer geneticist at the Sanger Institute, who has studied mutation rates in the early embryo. (Campbell was also behind the eyelid-skin study.) Our cells continue to accumulate mutations over a lifetime. A typical blood cell from a 100-year-old person, Vijg says, contains 4,000 single-letter mutations and possibly hundreds of other kinds of mutations that are more difficult to detect through single-cell sequencing. Cancer is more common in the elderly because they have simply had more time to accumulate the right—or rather, wrong—set of mutations.

"As humans age, cells in the body also become more different from each other. Perhaps half of your blood cells are descendants of a cell that acquired a certain mutation 20 years ago. The other half does not have this mutation. Imagine this process happening over and over again across decades, so that your body slowly becomes a mosaic of different cell groups, each with their unique mutations. We come to contain multitudes."

Comment: the mutations are there but so are the safety nets. Logically when DNA appeared the safety nets had to be there also, or life would not have continued. Only a designed system fits the facts. One can argue that a perfect designer would have made a perfect system that never mutated, but the way evolution advances is by having groups of cooperative genes creating new forms, which again would require a designer, and makes chance extremely unlikely.

Genome complexity: we survive constant mutations

by dhw, Saturday, May 12, 2018, 11:12 (2148 days ago) @ David Turell

DAVID’s comment: the mutations are there but so are the safety nets. Logically when DNA appeared the safety nets had to be there also, or life would not have continued. Only a designed system fits the facts. One can argue that a perfect designer would have made a perfect system that never mutated, but the way evolution advances is by having groups of cooperative genes creating new forms, which again would require a designer, and makes chance extremely unlikely.

Thank you for yet another amazing article on how cells work. And thank you also for your illuminating comment. If God exists, I would agree with you that he created a system whereby groups of cooperative cells (cell communities) created new forms, thus producing the whole higgledy-piggledy history of evolution. And I would also agree with you that he did not WANT a system that never mutated, because he WANTED the vast variety of forms that his invention has produced. It seems that our ideas about God and evolution are converging.

Genome complexity: we survive constant mutations

by David Turell @, Saturday, May 12, 2018, 14:44 (2148 days ago) @ dhw

DAVID’s comment: the mutations are there but so are the safety nets. Logically when DNA appeared the safety nets had to be there also, or life would not have continued. Only a designed system fits the facts. One can argue that a perfect designer would have made a perfect system that never mutated, but the way evolution advances is by having groups of cooperative genes creating new forms, which again would require a designer, and makes chance extremely unlikely.

dhw: Thank you for yet another amazing article on how cells work. And thank you also for your illuminating comment. If God exists, I would agree with you that he created a system whereby groups of cooperative cells (cell communities) created new forms, thus producing the whole higgledy-piggledy history of evolution. And I would also agree with you that he did not WANT a system that never mutated, because he WANTED the vast variety of forms that his invention has produced. It seems that our ideas about God and evolution are converging.

Thank you. We have never been far apart. My only point has been that if God bothered to create life He would have carefully monitored its progression, and I've agreed He might have given organisms an IM with guidelines or He dabbled

Genome complexity: we survive constant mutations

by dhw, Sunday, May 13, 2018, 13:45 (2147 days ago) @ David Turell

DAVID’s comment: the mutations are there but so are the safety nets. Logically when DNA appeared the safety nets had to be there also, or life would not have continued. Only a designed system fits the facts. One can argue that a perfect designer would have made a perfect system that never mutated, but the way evolution advances is by having groups of cooperative genes creating new forms, which again would require a designer, and makes chance extremely unlikely.

dhw: Thank you for yet another amazing article on how cells work. And thank you also for your illuminating comment. If God exists, I would agree with you that he created a system whereby groups of cooperative cells (cell communities) created new forms, thus producing the whole higgledy-piggledy history of evolution. And I would also agree with you that he did not WANT a system that never mutated, because he WANTED the vast variety of forms that his invention has produced. It seems that our ideas about God and evolution are converging.

DAVID: Thank you. We have never been far apart. My only point has been that if God bothered to create life He would have carefully monitored its progression, and I've agreed He might have given organisms an IM with guidelines or He dabbled.

There are still a few differences between us, but now that you have agreed that groups of cooperative cells (cell communities) created new forms, the gap has certainly narrowed. I would substitute “watched” for “carefully monitored”, and would suggest that if your God exists, he gave organisms an inventive mechanism without guidelines, though always with the proviso that he could dabble when he felt like it. I am delighted to see that in your theistic version of evolution you appear to have dropped the alternative that he equipped the first cells with computer programmes to be passed on for the millions of innovations, lifestyles and natural wonders that he did not dabble, and perhaps we may even agree that humans are special, but that the creation of new forms by the cooperating cell communities was not necessarily geared to the production of the sapiens brain. Or is that asking too much?

Genome complexity: we survive constant mutations

by David Turell @, Sunday, May 13, 2018, 15:10 (2147 days ago) @ dhw

DAVID’s comment: the mutations are there but so are the safety nets. Logically when DNA appeared the safety nets had to be there also, or life would not have continued. Only a designed system fits the facts. One can argue that a perfect designer would have made a perfect system that never mutated, but the way evolution advances is by having groups of cooperative genes creating new forms, which again would require a designer, and makes chance extremely unlikely.

dhw: Thank you for yet another amazing article on how cells work. And thank you also for your illuminating comment. If God exists, I would agree with you that he created a system whereby groups of cooperative cells (cell communities) created new forms, thus producing the whole higgledy-piggledy history of evolution. And I would also agree with you that he did not WANT a system that never mutated, because he WANTED the vast variety of forms that his invention has produced. It seems that our ideas about God and evolution are converging.

DAVID: Thank you. We have never been far apart. My only point has been that if God bothered to create life He would have carefully monitored its progression, and I've agreed He might have given organisms an IM with guidelines or He dabbled.

dhw: There are still a few differences between us, but now that you have agreed that groups of cooperative cells (cell communities) created new forms, the gap has certainly narrowed. I would substitute “watched” for “carefully monitored”, and would suggest that if your God exists, he gave organisms an inventive mechanism without guidelines, though always with the proviso that he could dabble when he felt like it. I am delighted to see that in your theistic version of evolution you appear to have dropped the alternative that he equipped the first cells with computer programmes to be passed on for the millions of innovations, lifestyles and natural wonders that he did not dabble, and perhaps we may even agree that humans are special, but that the creation of new forms by the cooperating cell communities was not necessarily geared to the production of the sapiens brain. Or is that asking too much?

God has purpose. He desired humans, as I view us a step beyond the rest of evolution. See the video I entered today. We live in the mind of God

Genome complexity: we survive constant mutations

by dhw, Monday, May 14, 2018, 12:57 (2146 days ago) @ David Turell

dhw: There are still a few differences between us, but now that you have agreed that groups of cooperative cells (cell communities) created new forms, the gap has certainly narrowed. I would substitute “watched” for “carefully monitored”, and would suggest that if your God exists, he gave organisms an inventive mechanism without guidelines, though always with the proviso that he could dabble when he felt like it. I am delighted to see that in your theistic version of evolution you appear to have dropped the alternative that he equipped the first cells with computer programmes to be passed on for the millions of innovations, lifestyles and natural wonders that he did not dabble, and perhaps we may even agree that humans are special, but that the creation of new forms by the cooperating cell communities was not necessarily geared to the production of the sapiens brain. Or is that asking too much?

DAVID: God has purpose. He desired humans, as I view us a step beyond the rest of evolution. See the video I entered today. We live in the mind of God.

If God exists, of course he has purpose. I agree that in terms of our consciousness we are a step beyond the rest of evolution. We may even be the result of a special dabble. I just don’t buy the hypotheses that a) every innovation, lifestyle and natural wonder had to be specially designed, and b) that all of them were geared to the production of your brain and mine. The video says nothing about the mind of God. It even suggests that we are the only observers. And frankly I have to admit that I am firmly convinced you exist and would continue to exist even if I popped off tomorrow.

Genome complexity: we survive constant mutations

by David Turell @, Monday, May 14, 2018, 17:22 (2146 days ago) @ dhw

dhw: There are still a few differences between us, but now that you have agreed that groups of cooperative cells (cell communities) created new forms, the gap has certainly narrowed. I would substitute “watched” for “carefully monitored”, and would suggest that if your God exists, he gave organisms an inventive mechanism without guidelines, though always with the proviso that he could dabble when he felt like it. I am delighted to see that in your theistic version of evolution you appear to have dropped the alternative that he equipped the first cells with computer programmes to be passed on for the millions of innovations, lifestyles and natural wonders that he did not dabble, and perhaps we may even agree that humans are special, but that the creation of new forms by the cooperating cell communities was not necessarily geared to the production of the sapiens brain. Or is that asking too much?

DAVID: God has purpose. He desired humans, as I view us a step beyond the rest of evolution. See the video I entered today. We live in the mind of God.

dhw: If God exists, of course he has purpose. I agree that in terms of our consciousness we are a step beyond the rest of evolution. We may even be the result of a special dabble. I just don’t buy the hypotheses that a) every innovation, lifestyle and natural wonder had to be specially designed, and b) that all of them were geared to the production of your brain and mine. The video says nothing about the mind of God. It even suggests that we are the only observers. And frankly I have to admit that I am firmly convinced you exist and would continue to exist even if I popped off tomorrow.

We've been over this before. The bush of life creates the balance of nature which supplies energy for evolution to last a very long time. An energy supply is required to maintain life preserve itself.

Genome complexity: we survive constant mutations

by dhw, Tuesday, May 15, 2018, 12:59 (2145 days ago) @ David Turell

DAVID: God has purpose. He desired humans, as I view us a step beyond the rest of evolution. See the video I entered today. We live in the mind of God.

dhw: If God exists, of course he has purpose. I agree that in terms of our consciousness we are a step beyond the rest of evolution. We may even be the result of a special dabble. I just don’t buy the hypotheses that a) every innovation, lifestyle and natural wonder had to be specially designed, and b) that all of them were geared to the production of your brain and mine. The video says nothing about the mind of God. It even suggests that we are the only observers. And frankly I have to admit that I am firmly convinced you exist and would continue to exist even if I popped off tomorrow.

DAVID: We've been over this before. The bush of life creates the balance of nature which supplies energy for evolution to last a very long time. An energy supply is required to maintain life preserve itself.

Yes indeed, life can’t go on without food. Nothing at all to do with (a) God having to design every single innovation, lifestyle and natural wonder himself, or (b) all of these being geared to the production of your brain and mine. We are in agreement.

Genome complexity: RNA controls in cells

by David Turell @, Friday, June 08, 2018, 19:37 (2121 days ago) @ dhw

RNA controls gene actions in cells and is shepherded around by RNA binding proteins:

https://phys.org/news/2018-06-decoding-rna-protein-interactions.html

"Although much has already been accomplished—mapping protein-DNA interactions and the inheritance of different epigenetic states—understanding the function of a DNA sequence also requires deciphering the purpose of the RNAs encoded by it, as well as which proteins bind to those RNAs.

"Such RNA-binding proteins (RBPs) regulate gene expression by controlling various post-transcriptional processes—directing where the RNAs go in the cell, how stable they are, and which proteins will be synthesized. Yet these vital RNA-protein relationships remain difficult to catalog, since most of the necessary experiments are arduous to complete and difficult to interpret accurately.

"In a new study, a team of MIT biologists and their collaborators describes the binding specificity of 78 human RBPs, using a one-step, unbiased method that efficiently and precisely determines the spectrum of RNA sequences and structures these proteins prefer. Their findings suggest that RBPs don't just recognize specific RNA segments, but are often influenced by contextual features as well—like the folded structures of the RNA in question, or the nucleotides flanking the RNA-binding sequence.

***

"From the moment an RNA is born, it is coated by RBPs that control nearly every aspect of its lifecycle. RBPs generally contain a binding domain, a three-dimensional folded structure that can attach to a specific nucleotide sequence on the RNA called a motif. Because there are over 1,500 different RBPs found in the human genome, the biologists needed a way to systematically determine which of those proteins bound to which RNA motifs.

***

"The researchers expected most RBPs to bind to a unique RNA motif, but to their surprise they found the opposite: Many of the proteins, regardless of structural class, seemed to prefer similar short, unfolded nucleotide sequence motifs.

"'Human cells express hundreds of thousands of distinct transcripts, so you might think that each RBP would bind a slightly different RNA sequence in order to distinguish between targets," Alexis says. "In fact, one might assume that having distinct RBP motifs would ensure maximum flexibility. But, as it turns out, nature has built in substantial redundancy; multiple proteins seem to bind the same short, linear sequences."

"This overlap in RBP binding preference suggested to the scientists that there must be some other indicator besides the sequence of the motif that signaled RBPs which RNA to target. Those signals, it turned out, stemmed from the spacing of the motifs as well as which nucleotide bases flank its binding sites. For the less common RBPs that targeted non-linear RNA sequences, the precise way the RNA folded also seemed to influence binding specificity.

"The obvious question, then, is: Why might RBPs have evolved to rely on contextual features instead of just giving them distinct motifs?

"Accessibility seems like one of the more plausible arguments. The researchers reasoned that linear RNA segments are physically easier to reach because they are not obstructed by other RNA strands, and they found that more accessible motifs are more likely to be bound. Another possibility is that having many proteins target the same motif creates some inter-protein competition. If one protein increases RNA stability and another decreases it, whichever binds the strongest will prevent the other from binding at all, enabling more pronounced changes in gene activity between cells or cell states. In other scenarios, proteins with similar functions that target the same motif could provide redundancy to ensure that regulation occurs in the cell."

"'It's definitely a difficult question, and one that we may never truly be able to answer," Dominguez says. "As RBPs duplicated over evolutionary time, perhaps altering recognition of the contextual features around the RNA motif was easier than changing the entire RNA motif. And that would give new opportunities for RBPs to select different cellular targets.'"

Comment: These studies are still working out all the feedback controls over using genome information properly in each cell. Our knowledge of the designed complexity of living cells increasingly demands that we recognized life is designed

Genome complexity: many different codes

by David Turell @, Thursday, June 14, 2018, 15:25 (2115 days ago) @ David Turell

At least 31 are listed. The code bases are the same with differing meanings in different organisms. Stop codons differ. See the website to have a clear picture of the real bush of life and to understand that the so-called tree is not a tree at the genome level:

https://www.ncbi.nlm.nih.gov/Taxonomy/taxonomyhome.html/index.cgi?chapter=cgencodes

Here is a commentary:

Biologists have long thought that the genetic code is basically the same in all living organ isms-that is, genes “code for” the same protein in almost identical ways in almost all living things. As our SOS discussion illustrated, it is difficult to see how the codon-amino acid assignments could change without killing the host organism. That’s why evolutionary biologists have argued that the code we have today is the same as the code in the first living organism and why a universal genetic code points to a universal common ancestor. But is the genetic code universal? It turns out that it’s not. Since 1985 molecular biologists have discovered at least 18 different genetic codes in various species. Many of these are significantly different from the standard code. For example, the standard code has three different mRNA stop codons: UGA, UAA, and UAG . (A “stop codon” tells the cell to stop building-the protein is complete.) However, some variant codes have only one stop codon, UGA. The other “universal” stop codons now code for the amino acid glutamine. It’s very hard to see how an organism could have survived a transformation from the standard code to this one. Changing to this new code would cause the cell to produce useless strings of extra amino acids when it should have stopped protein production.”

Site: https://uncommondescent.com/evolution/there-are-now-many-variants-of-the-universal-gene...

My Comment: Does common descent exist? For an alternative code to work, design is required.

Genome complexity: complex traits may involve all genes

by David Turell @, Friday, June 22, 2018, 18:19 (2107 days ago) @ David Turell

A new complex theory about core genes and how certain traits might involve all genes:

https://www.quantamagazine.org/disease-networks-show-molecular-connections-20150129/

"Starting about 15 years ago, geneticists began to collect DNA from thousands of people who shared traits, to look for clues to each trait’s cause in commonalities between their genomes, a kind of analysis called a genome-wide association study (GWAS). ...The conclusion, sometimes called the polygenic hypothesis, was that multiple loci, or positions in the genome, were likely to be involved in every trait, with each contributing just a small part.

***

"The authors described what they called the “omnigenic” model of complex traits. Drawing on GWAS analyses of three diseases, they concluded that in the cell types that are relevant to a disease, it appears that not 15, not 100, but essentially all genes contribute to the condition. The authors suggested that for some traits, “multiple” loci could mean more than 100,000.

***

"The origin of the idea lies in a very simple observation: When you look at the portions of the genome that GWAS findings have flagged as significant to individual traits, they are eerily well-distributed. Pritchard and his colleagues had been studying loci that contribute to height in humans. “What we realized was that the signal for height was coming from almost the whole genome,” he said. If the genome were a long string of ornamental lights, and every DNA snippet linked to height were illuminated, more than 100,000 lights would be shining all the way down the string. That result contrasted starkly with the general expectation that GWAS findings would be clustered around the most important genes for a trait.

***

"But when the researchers looked at disease-specific cell types, an enormous number of the regions flagged by GWAS were not in those genes. They were in genes expressed in nearly every cell in the body — genes doing basic maintenance tasks that all cells need. Pritchard and his colleagues suggest that this manifests a truth that is perhaps not always taken literally: Everything in a cell is connected. If incremental disruptions in basic processes can add up to greatly derange a trait, then perhaps nearly every gene expressed in a cell, no matter how seemingly unrelated to the metabolic process of interest, matters.

***

"it may be fruitful to think of the genes in a cell as a network. There may be some very highly connected genes at the center of a disease process, which they dub core genes. Peripheral genes, meanwhile, in aggregate help tip the scales one way or the other. The Cell paper authors suggest that understanding of the core genes will offer the best insights into the mechanism of a disease. Piecing together how peripheral genes contribute, on the other hand, will broaden understanding of why some people develop a disorder and others don’t.

"Since the Cell paper’s publication a year ago, scientists’ discussion has circled around whether such a distinction is useful. David Goldstein, a geneticist at Columbia University, is not sure that disease processes must truly be routed through core genes, but he also says that the idea that not everything picked up by GWAS is central and specific to a given disease is important.

***

" according to Naomi Wray, a quantitative geneticist at the University of Queensland who pointed out when scientists first started doing GWAS analyses that they should expect to see many weak associations. A few conditions, she says, are primarily attributable to a small number of identifiable genes, or even just one — yet other genes may still flip the switch between one manifestation of illness and another. She cites the example of Huntington’s disease, a progressive neurological disorder caused by a specific defect in one gene. .. Scientists in the field are looking at other loci linked to Huntington’s disease to see how they might be causing the differences.

“'These [loci] are by definition in peripheral genes. But they’re actually how the body is responding to this major insult of the core gene,” Wray said.

***

"Franke, who sees the paper as a provocatively phrased extension of earlier ideas, says that it has nevertheless shaped her thinking in the past year. “It made me rethink what I know about signal transduction — about how messages are relayed in cells — and how functions are fulfilled,” she said. The deeper you look at the workings of a cell, the more you realize that a single common protein may have quite different effects depending on what type of cell it is in: It may bear different messages, or block different processes, so much so that traits that might seem to be quite disconnected begin to change."

Comment: It is obvious that DNA must be studied in 3-D and in groups of genes and their effects. DNA does not simply code for proteins.

Genome complexity: RNA modifications

by David Turell @, Wednesday, July 11, 2018, 22:03 (2088 days ago) @ David Turell

There seems to be another level of encryption involving RNA coding:

https://evolutionnews.org/2018/07/encryption-system-found-in-genes/

"RNA modifications can encrypt the RNA code and are responsible for a very sophisticated control of RNA function. A Danish-German research team has shown that modified RNA bases have a great impact on the dynamics of gene expression from DNA to functional RNA. The study yields important new insight into how the basis of RNA modifications can affect the function of mature RNA molecules.

***

"The research-team has focused on the RNA-modification m6A and shown that RNA can be labeled with this modification while being copied from DNA…. The results demonstrate that an m6A positioned at an exon next to an intron increases the RNA maturation process, while m6A within the introns slows down the maturation of RNA.

***

"Newly made RNA consists of functional parts (exons) and non-functional parts (introns). Introns are excised in a process called splicing to yield a mature and functional RNA molecule composes [sic] entirely of exons. The RNA modification m6A can increase or inhibit this maturation process dependent of where m6A is deposited on newly made RNA.

"It has long been a mystery why genes code for stretches called introns that are translated but then cut out afterwards. Why are they there? Here’s where the findings get really interesting. Introns appear to help scramble the message, fulfilling the encryption role, but they do something else: they regulate how the exons will be assembled. The paper in Cell Reports explains how it works:

"Here, we provide a time-resolved high-resolution assessment of m6A on nascent RNA transcripts and unveil its importance for the control of RNA splicing kinetics. We find that early co-transcriptional m6A deposition near splice junctions promotes fast splicing, while m6A modifications in introns are associated with long, slowly processed introns and alternative splicing events. In conclusion, we show that early m6A deposition specifies the fate of transcripts regarding splicing kinetics and alternative splicing.

***

"according to the scientists at Aarhus, the specific position of the m6a mark appears highly relevant not only to the type of messenger RNA produced — and thus the protein to be translated — but also to the rate of production. If the m6a mark is placed near a splice junction, the constitutive transcript is produced quickly (i.e., exons are arranged in the order they were transcribed). If the mark is placed on an intron, it slows down the splicing, and might produce a completely different transcript with a different protein resulting. Is this a method to achieve cell-specific regulation?

"Our January 2017 article spoke of the m6a process as a kind of “if-then” algorithm: i.e., if this gene is found in a muscle cell, transcribe it this way; if found in a nerve cell, transcribe it another way, and so on. For this to work, the gene must embed the key in its introns, and the associated m6a marker must know the key to arrange the transcript accordingly. The researchers found that 57 percent of the markers were found on introns, and another 9 percent are on untranslated regions. Only 22 percent were found in coding regions.

"It’s not just having the mark that directs the regulation. Previous research identified a “protein family called m6A readers, which recognize and bind specifically to sequences marked with m6A.” In addition, there are FTO pathways that respond to m6a position to either include or exclude certain exons in the transcript. We can see the encryption algorithm coming into focus: genes employ a key to embed introns and m6a markers, and certain readers that know the key respond according to this extra information.

"Our study shows that the crucial role of m6A on SED [splicing efficiency dynamics] as well as on alternative splicing is position dependent. m6A deposited in intronic regions sort transcripts to a slow-track processing pathway and is associated with alternative splicing while m6A deposited at exonic boundaries of SJs sort transcripts to a fast-track processing pathway and constitutive splicing."

Comment: Just an other example of the multiple layers of gene control. But it dos not tell us how life fully codes for homeostasis which it obviously able to do.

Genome complexity: RNA modifications

by Balance_Maintained @, U.S.A., Thursday, July 12, 2018, 02:06 (2088 days ago) @ David Turell

Notice that it called it an if-then statement. This bolsters my theory of a designed programming language.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: RNA modifications

by David Turell @, Thursday, July 12, 2018, 15:24 (2087 days ago) @ Balance_Maintained

Tony: Notice that it called it an if-then statement. This bolsters my theory of a designed programming language.

I can only agree.

Genome complexity: Removing foreign or damaged DNA

by David Turell @, Thursday, July 12, 2018, 22:08 (2087 days ago) @ David Turell

Cells have to protect themselves from damaged DNA and foreign DNA:

https://phys.org/news/2018-07-scientists-decipher-key-features-critical.html

"The human body is built for survival. Each one of its cells is closely guarded by a set of immune proteins armed with nearly foolproof radars that detect foreign or damaged DNA.

"One of the cells' most critical sentinels is a "first responder" protein known as cGAS, which senses the presence of foreign and cancerous DNA and initiates a signaling cascade that triggers the body's defenses.

***

"Specifically, the research shows that human cGAS harbors mutations that make it exquisitely sensitive to long lengths of DNA but render it "blind" or "insensitive" to short DNA fragments.

"'Human cGAS is a highly discriminating protein that has evolved enhanced specificity toward DNA," said co-first author Aaron Whiteley,

"In all mammals, cGAS works by detecting DNA that's in the wrong place. Under normal conditions, DNA is tightly packed and protected in the cell's nucleus—the cellular "safe"—where genetic information is stored. DNA has no business roaming freely around the cell. When DNA fragments do end up outside the nucleus and in the cell's cytosol, the liquid that encases the cell's organelles, it's usually a sign that something ominous is afoot, such as damage coming from within the cell or foreign DNA from viruses or bacteria that has made its way into the cell.

"The cGAS protein works by recognizing such misplaced DNA. Normally, it lies dormant in cells. But as soon as it senses the presence of DNA outside the nucleus, cGAS springs into action. It makes another chemical—a second messenger—called cGAMP, thus setting in motion a molecular chain reaction that alerts the cell to the abnormal presence of DNA. At the end of this signaling reaction, the cell either gets repaired or, if damaged beyond repair, it self-destructs.

"But the health and integrity of the cell are predicated on cGAS' ability to distinguish harmless DNA from foreign DNA or self-DNA released during cell damage and stress.

"It's a fine balancing act that keeps the immune system in equilibrium. An overactive cGAS can spark autoimmunity, or self-attack, while cGAS that fails to detect foreign DNA can lead to tumor growth and cancer development," said co-first author Wen Zhou, a postdoctoral researcher at Harvard Medical School and Dana-Farber Cancer Institute.

***

"The experiments revealed that out of the 116 amino acids that differ in human and mouse cGAS, only two accounted for the altered function of human cGAS. Indeed, human cGAS was capable of recognizing long DNA with great precision but it ignored short DNA fragments. The mouse version of the protein, by contrast, did not differentiate between long and short DNA fragments.

"'These two tiny amino acids make a world of difference," Whiteley said. "They allow the human protein to be highly selective and respond only to long DNA, while ignoring short DNA, essentially rendering the human protein more tolerant of DNA presence in the cytosol of the cell."

"Plotting the genetic divergence on an evolutionary timescale, the scientists determined that the human and mouse cGAS genes parted ways sometime between 10 million and 15 million years ago.

"The two amino acids responsible for sensing long DNA and tolerating short DNA are found solely in humans and nonhuman primates, such as gorillas, chimps and bonobos."

Comment: It is obvious that damaged or foreign DNA must be stopped at all times. Therefore this cellular defense, or some other form of it, was designed along with the appearance of DNA coding or life would not have continued from the moment it began..

Genome complexity: Removing foreign or damaged DNA

by Balance_Maintained @, U.S.A., Thursday, July 12, 2018, 23:49 (2087 days ago) @ David Turell

Cells have to protect themselves from damaged DNA and foreign DNA:

https://phys.org/news/2018-07-scientists-decipher-key-features-critical.html

"The human body is built for survival. Each one of its cells is closely guarded by a set of immune proteins armed with nearly foolproof radars that detect foreign or damaged DNA.

"One of the cells' most critical sentinels is a "first responder" protein known as cGAS, which senses the presence of foreign and cancerous DNA and initiates a signaling cascade that triggers the body's defenses.

***

"Specifically, the research shows that human cGAS harbors mutations that make it exquisitely sensitive to long lengths of DNA but render it "blind" or "insensitive" to short DNA fragments.

"'Human cGAS is a highly discriminating protein that has evolved enhanced specificity toward DNA," said co-first author Aaron Whiteley,

"In all mammals, cGAS works by detecting DNA that's in the wrong place. Under normal conditions, DNA is tightly packed and protected in the cell's nucleus—the cellular "safe"—where genetic information is stored. DNA has no business roaming freely around the cell. When DNA fragments do end up outside the nucleus and in the cell's cytosol, the liquid that encases the cell's organelles, it's usually a sign that something ominous is afoot, such as damage coming from within the cell or foreign DNA from viruses or bacteria that has made its way into the cell.

"The cGAS protein works by recognizing such misplaced DNA. Normally, it lies dormant in cells. But as soon as it senses the presence of DNA outside the nucleus, cGAS springs into action. It makes another chemical—a second messenger—called cGAMP, thus setting in motion a molecular chain reaction that alerts the cell to the abnormal presence of DNA. At the end of this signaling reaction, the cell either gets repaired or, if damaged beyond repair, it self-destructs.

"But the health and integrity of the cell are predicated on cGAS' ability to distinguish harmless DNA from foreign DNA or self-DNA released during cell damage and stress.

"It's a fine balancing act that keeps the immune system in equilibrium. An overactive cGAS can spark autoimmunity, or self-attack, while cGAS that fails to detect foreign DNA can lead to tumor growth and cancer development," said co-first author Wen Zhou, a postdoctoral researcher at Harvard Medical School and Dana-Farber Cancer Institute.

***

"The experiments revealed that out of the 116 amino acids that differ in human and mouse cGAS, only two accounted for the altered function of human cGAS. Indeed, human cGAS was capable of recognizing long DNA with great precision but it ignored short DNA fragments. The mouse version of the protein, by contrast, did not differentiate between long and short DNA fragments.

"'These two tiny amino acids make a world of difference," Whiteley said. "They allow the human protein to be highly selective and respond only to long DNA, while ignoring short DNA, essentially rendering the human protein more tolerant of DNA presence in the cytosol of the cell."

"Plotting the genetic divergence on an evolutionary timescale, the scientists determined that the human and mouse cGAS genes parted ways sometime between 10 million and 15 million years ago.

"The two amino acids responsible for sensing long DNA and tolerating short DNA are found solely in humans and nonhuman primates, such as gorillas, chimps and bonobos."

David Comment: It is obvious that damaged or foreign DNA must be stopped at all times. Therefore this cellular defense, or some other form of it, was designed along with the appearance of DNA coding or life would not have continued from the moment it began..


Functionally, tt would also prevent half-cocked additions of non-sensical DNA from foreign sources as well, preventing gradualism from occuring by methods such as horizontal gene transfer.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: Removing foreign or damaged DNA

by David Turell @, Friday, July 13, 2018, 00:59 (2087 days ago) @ Balance_Maintained

Cells have to protect themselves from damaged DNA and foreign DNA:

https://phys.org/news/2018-07-scientists-decipher-key-features-critical.html

David Comment: It is obvious that damaged or foreign DNA must be stopped at all times. Therefore this cellular defense, or some other form of it, was designed along with the appearance of DNA coding or life would not have continued from the moment it began..

Tony: Functionally, it would also prevent half-cocked additions of non-sensical DNA from foreign sources as well, preventing gradualism from occurring by methods such as horizontal gene transfer.

But horizontal transfer seems to be one of the ways evolution has progressed. I've just presented that.

Genome complexity: Removing foreign or damaged DNA

by Balance_Maintained @, U.S.A., Friday, July 13, 2018, 03:00 (2087 days ago) @ David Turell
edited by Balance_Maintained, Friday, July 13, 2018, 03:10

Cells have to protect themselves from damaged DNA and foreign DNA:

https://phys.org/news/2018-07-scientists-decipher-key-features-critical.html

David Comment: It is obvious that damaged or foreign DNA must be stopped at all times. Therefore this cellular defense, or some other form of it, was designed along with the appearance of DNA coding or life would not have continued from the moment it began..

Tony: Functionally, it would also prevent half-cocked additions of non-sensical DNA from foreign sources as well, preventing gradualism from occurring by methods such as horizontal gene transfer.


David : But horizontal transfer seems to be one of the ways evolution has progressed. I've just presented that.


Stop and think about this. The story of horizontal gene transfer is based on finding the same or similar genes inside separate species. This forces them to make up stories about how it happened. They have no evidence that it happened, but it is required to explain their data within the framework of evolution. This screws with timelines and cladistics. The just so story of mosquito transfer is not backed by evidence. Moreover, this safeguard would prevent horizontal transfer

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: Removing foreign or damaged DNA

by David Turell @, Friday, July 13, 2018, 18:31 (2086 days ago) @ Balance_Maintained

David : But horizontal transfer seems to be one of the ways evolution has progressed. I've just presented that.


Tony:Stop and think about this. The story of horizontal gene transfer is based on finding the same or similar genes inside separate species. This forces them to make up stories about how it happened. They have no evidence that it happened, but it is required to explain their data within the framework of evolution. This screws with timelines and cladistics. The just so story of mosquito transfer is not backed by evidence. Moreover, this safeguard would prevent horizontal transfer.

I am delighted with your skepticism. However the article below accepts that the transfers do occur in bacteria and similar simple celled animals. I agree with you that in complex multicellular it can be questioned, because genes can have multiple results in appearance and in activity with the slicing and dicing by the interpretive mechanisms in the genome. On the other hand DNA is huge within amoeba, longer than ours but with the same bases, so just rearrangement can make a gene look like someone else's gene. The article uses transfer by parasite bites, viruses, etc . to explain it, because it is hard to imagine my horses' genes jumping into me. The article is long but informative and I've entered it before here, but on our site is will not reproduce, so I looked it up again:

https://aeon.co/essays/genes-that-jump-species-does-this-shake-the-tree-of-life

jumping genes

by dhw, Saturday, July 14, 2018, 12:01 (2085 days ago) @ David Turell

You posted this on an unrelated thread, so I've brought it back under a different title.


DAVID: [...] horizontal transfer seems to be one of the ways evolution has progressed. I've just presented that. The article uses transfer by parasite bites, viruses, etc . to explain it, because it is hard to imagine my horses' genes jumping into me. The article is long but informative and I've entered it before here, but on our site is will not reproduce, so I looked it up again:


https://aeon.co/essays/genes-that-jump-species-does-this-shake-the-tree-of-life


Thank you for this. I’ve taken the liberty of extracting quotes which seem to me to offer scientific evidence for natural means of innovation, and for the whole process of cellular cooperation as a driving force for evolution.

QUOTES:

It seems that the genome of just about every modern species is something of a mosaic constructed with genes borrowed from many different forms of life.

McClintock’s pioneering work demonstrated for the first time that a genome is highly dynamic, not forever fixed in one order.

Now it seems our own genome is a patchwork of raw genetic material coming from different places with different histories – that to me is very profound. Even the largest eukaryote genomes have this patchwork origin to them.’

In a surprising number of instances, however, wayfaring genes make a new life for themselves, becoming successful enough to change the way an organism behaves and steer its evolution.

In some cases, this genetic hopscotching ‘could exert a very powerful evolutionary force’, says Li. ‘It can introduce novelties that cannot be achieved by gradual genetic mutations.’

Horizontal gene transfer opens the possibility of a creature instantaneously acquiring a gene-trait combo that its own genome would have been unlikely to invent by itself.

Rather than evolving from one ‘last universal ancestor’, all life arose from a communal pool of primitive cells with unbridled zeal for exchanging DNA

jumping genes

by David Turell @, Saturday, July 14, 2018, 18:51 (2085 days ago) @ dhw

dhw: You posted this on an unrelated thread, so I've brought it back under a different title.


DAVID: [...] horizontal transfer seems to be one of the ways evolution has progressed. I've just presented that. The article uses transfer by parasite bites, viruses, etc . to explain it, because it is hard to imagine my horses' genes jumping into me. The article is long but informative and I've entered it before here, but on our site is will not reproduce, so I looked it up again:


https://aeon.co/essays/genes-that-jump-species-does-this-shake-the-tree-of-life

dhw: Thank you for this. I’ve taken the liberty of extracting quotes which seem to me to offer scientific evidence for natural means of innovation, and for the whole process of cellular cooperation as a driving force for evolution.

QUOTES:

It seems that the genome of just about every modern species is something of a mosaic constructed with genes borrowed from many different forms of life.

McClintock’s pioneering work demonstrated for the first time that a genome is highly dynamic, not forever fixed in one order.

Now it seems our own genome is a patchwork of raw genetic material coming from different places with different histories – that to me is very profound. Even the largest eukaryote genomes have this patchwork origin to them.’

In a surprising number of instances, however, wayfaring genes make a new life for themselves, becoming successful enough to change the way an organism behaves and steer its evolution.

In some cases, this genetic hopscotching ‘could exert a very powerful evolutionary force’, says Li. ‘It can introduce novelties that cannot be achieved by gradual genetic mutations.’

Horizontal gene transfer opens the possibility of a creature instantaneously acquiring a gene-trait combo that its own genome would have been unlikely to invent by itself.

Rather than evolving from one ‘last universal ancestor’, all life arose from a communal pool of primitive cells with unbridled zeal for exchanging DNA

All of these quotes build a picture of the majority of information in the genome was pressent from the beginning and just rearranged in the code of DNA.

jumping genes

by Balance_Maintained @, U.S.A., Sunday, July 15, 2018, 04:54 (2084 days ago) @ David Turell

dhw: You posted this on an unrelated thread, so I've brought it back under a different title.


DAVID: [...] horizontal transfer seems to be one of the ways evolution has progressed. I've just presented that. The article uses transfer by parasite bites, viruses, etc . to explain it, because it is hard to imagine my horses' genes jumping into me. The article is long but informative and I've entered it before here, but on our site is will not reproduce, so I looked it up again:


https://aeon.co/essays/genes-that-jump-species-does-this-shake-the-tree-of-life

dhw: Thank you for this. I’ve taken the liberty of extracting quotes which seem to me to offer scientific evidence for natural means of innovation, and for the whole process of cellular cooperation as a driving force for evolution.

QUOTES:

It seems that the genome of just about every modern species is something of a mosaic constructed with genes borrowed from many different forms of life.

McClintock’s pioneering work demonstrated for the first time that a genome is highly dynamic, not forever fixed in one order.

Now it seems our own genome is a patchwork of raw genetic material coming from different places with different histories – that to me is very profound. Even the largest eukaryote genomes have this patchwork origin to them.’

In a surprising number of instances, however, wayfaring genes make a new life for themselves, becoming successful enough to change the way an organism behaves and steer its evolution.

In some cases, this genetic hopscotching ‘could exert a very powerful evolutionary force’, says Li. ‘It can introduce novelties that cannot be achieved by gradual genetic mutations.’

Horizontal gene transfer opens the possibility of a creature instantaneously acquiring a gene-trait combo that its own genome would have been unlikely to invent by itself.

Rather than evolving from one ‘last universal ancestor’, all life arose from a communal pool of primitive cells with unbridled zeal for exchanging DNA


David: All of these quotes build a picture of the majority of information in the genome was pressent from the beginning and just rearranged in the code of DNA.

What it sounds like to to me is "We have no effing clue what the hell is going on....now we have problems common descent can't explain so we have to have numerous original ancestor species with all the genetic code for all life already in them, and a way for DNA to jump around..."

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

jumping genes

by David Turell @, Sunday, July 15, 2018, 15:07 (2084 days ago) @ Balance_Maintained

dhw: You posted this on an unrelated thread, so I've brought it back under a different title.


DAVID: [...] horizontal transfer seems to be one of the ways evolution has progressed. I've just presented that. The article uses transfer by parasite bites, viruses, etc . to explain it, because it is hard to imagine my horses' genes jumping into me. The article is long but informative and I've entered it before here, but on our site is will not reproduce, so I looked it up again:


https://aeon.co/essays/genes-that-jump-species-does-this-shake-the-tree-of-life

dhw: Thank you for this. I’ve taken the liberty of extracting quotes which seem to me to offer scientific evidence for natural means of innovation, and for the whole process of cellular cooperation as a driving force for evolution.

QUOTES:

It seems that the genome of just about every modern species is something of a mosaic constructed with genes borrowed from many different forms of life.

McClintock’s pioneering work demonstrated for the first time that a genome is highly dynamic, not forever fixed in one order.

Now it seems our own genome is a patchwork of raw genetic material coming from different places with different histories – that to me is very profound. Even the largest eukaryote genomes have this patchwork origin to them.’

In a surprising number of instances, however, wayfaring genes make a new life for themselves, becoming successful enough to change the way an organism behaves and steer its evolution.

In some cases, this genetic hopscotching ‘could exert a very powerful evolutionary force’, says Li. ‘It can introduce novelties that cannot be achieved by gradual genetic mutations.’

Horizontal gene transfer opens the possibility of a creature instantaneously acquiring a gene-trait combo that its own genome would have been unlikely to invent by itself.

Rather than evolving from one ‘last universal ancestor’, all life arose from a communal pool of primitive cells with unbridled zeal for exchanging DNA


David: All of these quotes build a picture of the majority of information in the genome was pressent from the beginning and just rearranged in the code of DNA.


Tony: What it sounds like to to me is "We have no effing clue what the hell is going on....now we have problems common descent can't explain so we have to have numerous original ancestor species with all the genetic code for all life already in them, and a way for DNA to jump around..."

What it means to me is more evidence God dabbled when needed.

Genome complexity: control of alternate start sites

by David Turell @, Monday, July 16, 2018, 21:08 (2083 days ago) @ David Turell

Depending the start site the coding for protein may produce a different product:

https://phys.org/news/2018-07-hidden-rnas-protein-synthesis.html

"While scanning RNAs for the first AUG, the protein-making machinery frequently encounters sites that diverge from AUG by one building block (such as AUA). On occasion, protein synthesis starts from such alternative start sites. How the protein-making machinery chooses which alternative sites to use has been a mystery.

"In a new study published in Nature, scientists describe how the protein-making machinery identifies alternative initiation sites from which to start protein synthesis. "We discovered a mechanism that explains how sites are chosen for translation events that occur in regions that are traditionally considered untranslated and that initiate at non-traditional start sites," said senior author Eckhard Jankowsky, Ph.D. "Over the last several years it has become clear that translation in these regions is pervasive, but it is poorly understood how start sites are chosen among the millions of possible start sites."

"In the new study, Jankowsky's team leveraged an enzyme that is part of the protein-making machinery—called Ded1p. Mutations in the human version of Ded1p are linked to tumors and cognitive disabilities. Viruses often target the critical enzyme to disrupt protein synthesis inside cells. Jankowsky's team created yeast cells with defective Ded1p. The use of alternative start sites for protein synthesis, like AUA or AAG, dramatically increased in these cells. However, the cells only used a small fraction of possible alternative sites.

"The researchers found that chosen alternative start sites were next to regions where the RNA folds back on itself. Ded1p is an RNA helicase—an enzyme that unzips folded RNA structures—but if it is defective it is unable to do so. If left folded, RNA structures stall scanning by the protein-making machinery and cause protein synthesis from an alternative start site nearby. "Our findings reveal a simple mechanism that involves RNA structure and a helicase." Jankowsky said. "If an alternative initiation site is close to RNA structure, it is used to start protein synthesis. So RNA structure and alternative initiation sites together are the signal to start protein production from non-traditional sites."

"Since Ded1p is present in all organisms, the findings are likely universally applicable. Protein synthesis starting from alternative translation initiation sites often impacts production of main proteins, encoded after AUG strings in the RNA, and thereby determines protein balance inside cells. "

Comment: just another level of control which means one gene can make several different proteins.

Genome complexity: control of alternate start sites

by Balance_Maintained @, U.S.A., Tuesday, July 17, 2018, 05:52 (2082 days ago) @ David Turell

Depending the start site the coding for protein may produce a different product:

https://phys.org/news/2018-07-hidden-rnas-protein-synthesis.html

"While scanning RNAs for the first AUG, the protein-making machinery frequently encounters sites that diverge from AUG by one building block (such as AUA). On occasion, protein synthesis starts from such alternative start sites. How the protein-making machinery chooses which alternative sites to use has been a mystery.

"In a new study published in Nature, scientists describe how the protein-making machinery identifies alternative initiation sites from which to start protein synthesis. "We discovered a mechanism that explains how sites are chosen for translation events that occur in regions that are traditionally considered untranslated and that initiate at non-traditional start sites," said senior author Eckhard Jankowsky, Ph.D. "Over the last several years it has become clear that translation in these regions is pervasive, but it is poorly understood how start sites are chosen among the millions of possible start sites."

"In the new study, Jankowsky's team leveraged an enzyme that is part of the protein-making machinery—called Ded1p. Mutations in the human version of Ded1p are linked to tumors and cognitive disabilities. Viruses often target the critical enzyme to disrupt protein synthesis inside cells. Jankowsky's team created yeast cells with defective Ded1p. The use of alternative start sites for protein synthesis, like AUA or AAG, dramatically increased in these cells. However, the cells only used a small fraction of possible alternative sites.

"The researchers found that chosen alternative start sites were next to regions where the RNA folds back on itself. Ded1p is an RNA helicase—an enzyme that unzips folded RNA structures—but if it is defective it is unable to do so. If left folded, RNA structures stall scanning by the protein-making machinery and cause protein synthesis from an alternative start site nearby. "Our findings reveal a simple mechanism that involves RNA structure and a helicase." Jankowsky said. "If an alternative initiation site is close to RNA structure, it is used to start protein synthesis. So RNA structure and alternative initiation sites together are the signal to start protein production from non-traditional sites."

"Since Ded1p is present in all organisms, the findings are likely universally applicable. Protein synthesis starting from alternative translation initiation sites often impacts production of main proteins, encoded after AUG strings in the RNA, and thereby determines protein balance inside cells. "

David Comment: just another level of control which means one gene can make several different proteins.

And one that acts as a defensive mechanism for the cell, it seems. On one level, the one observed thus far, it prevents defective proteins from forming. However, the article methions that cells do this in response to viral targeting as well, which indicates to me that it might also be a low level part of the immune system. Could this be another level of viral intruder detection? If so, could the new proteins, the one generated from the alternative start site, actually act as a trigger for alerting the immune system that something got by them, and informing it of what they virus is targeting so that the immune system can respond appropriately?

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: control of alternate start sites

by David Turell @, Tuesday, July 17, 2018, 15:20 (2082 days ago) @ Balance_Maintained

Depending the start site the coding for protein may produce a different product:

https://phys.org/news/2018-07-hidden-rnas-protein-synthesis.html

"While scanning RNAs for the first AUG, the protein-making machinery frequently encounters sites that diverge from AUG by one building block (such as AUA). On occasion, protein synthesis starts from such alternative start sites. How the protein-making machinery chooses which alternative sites to use has been a mystery.

"In a new study published in Nature, scientists describe how the protein-making machinery identifies alternative initiation sites from which to start protein synthesis. "We discovered a mechanism that explains how sites are chosen for translation events that occur in regions that are traditionally considered untranslated and that initiate at non-traditional start sites," said senior author Eckhard Jankowsky, Ph.D. "Over the last several years it has become clear that translation in these regions is pervasive, but it is poorly understood how start sites are chosen among the millions of possible start sites."

David Comment: just another level of control which means one gene can make several different proteins.


Tony: And one that acts as a defensive mechanism for the cell, it seems. On one level, the one observed thus far, it prevents defective proteins from forming. However, the article methions that cells do this in response to viral targeting as well, which indicates to me that it might also be a low level part of the immune system. Could this be another level of viral intruder detection? If so, could the new proteins, the one generated from the alternative start site, actually act as a trigger for alerting the immune system that something got by them, and informing it of what they virus is targeting so that the immune system can respond appropriately?

Your thought makes sense.

Genome complexity: a new DNA repair mechanism found

by David Turell @, Wednesday, July 18, 2018, 20:13 (2081 days ago) @ David Turell

It has several moving parts to bring ends together:

https://medicalxpress.com/news/2018-07-scientists-uncover-dna-shield-crucial.html

"Scientists have made a major discovery about how cells repair broken strands of DNA that could have huge implications for the treatment of cancer.

Their study, published in Nature today, uncovered a brand new protein complex in cells that shields broken DNA ends and controls the way in which it is repaired.

***

"The newly named 'Shieldin' complex was also found to be important for generating the right type of antibodies during an immune response, and mutations could lead to immune-related disorders.

***

"In healthy cells, the complex was found to attach to the ends of broken DNA so that the 'blunt ends' of the DNA have to be stuck back together directly—a quicker, messier way of repairing DNA that can sometimes be necessary for making antibodies during immune responses.
When the researchers introduced mutations into the Shieldin complex—which stop it from forming and protecting broken DNA ends—cells are free to repair DNA via a different method, and this means PARP inhibitors are no longer effective.

***

"'Our study reveals for the first time a complex that is crucial for DNA repair."

Abstract: https://www.nature.com/articles/s41586-018-0340-7

"53BP1 is a chromatin-binding protein that regulates the repair of DNA double-strand breaks by suppressing the nucleolytic resection of DNA termini1,2. This function of 53BP1 requires interactions with PTIP3 and RIF14,5,6,7,8,9, the latter of which recruits REV7 (also known as MAD2L2) to break sites10,11. How 53BP1-pathway proteins shield DNA ends is currently unknown, but there are two models that provide the best potential explanation of their action. In one model the 53BP1 complex strengthens the nucleosomal barrier to end-resection nucleases12,13, and in the other 53BP1 recruits effector proteins with end-protection activity. Here we identify a 53BP1 effector complex, shieldin, that includes C20orf196 (also known as SHLD1), FAM35A (SHLD2), CTC-534A2.2 (SHLD3) and REV7. Shieldin localizes to double-strand-break sites in a 53BP1- and RIF1-dependent manner, and its SHLD2 subunit binds to single-stranded DNA via OB-fold domains that are analogous to those of RPA1 and POT1. Loss of shieldin impairs non-homologous end-joining, leads to defective immunoglobulin class switching and causes hyper-resection. Mutations in genes that encode shieldin subunits also cause resistance to poly(ADP-ribose) polymerase inhibition in BRCA1-deficient cells and tumours, owing to restoration of homologous recombination. Finally, we show that binding of single-stranded DNA by SHLD2 is critical for shieldin function, consistent with a model in which shieldin protects DNA ends to mediate 53BP1-dependent DNA repair."

Comment: Sorry there is no diagram. This is a very complex system of various proteins which had to be designed when DNA was designed. DNA repair is crucial for the survival of life. That there is more than one system indicates how important repair is.

Genome complexity: a new DNA repair mechanism found

by Balance_Maintained @, U.S.A., Thursday, July 19, 2018, 06:33 (2080 days ago) @ David Turell

It has several moving parts to bring ends together:

https://medicalxpress.com/news/2018-07-scientists-uncover-dna-shield-crucial.html

"Scientists have made a major discovery about how cells repair broken strands of DNA that could have huge implications for the treatment of cancer.

Their study, published in Nature today, uncovered a brand new protein complex in cells that shields broken DNA ends and controls the way in which it is repaired.

***

"The newly named 'Shieldin' complex was also found to be important for generating the right type of antibodies during an immune response, and mutations could lead to immune-related disorders.

***

"In healthy cells, the complex was found to attach to the ends of broken DNA so that the 'blunt ends' of the DNA have to be stuck back together directly—a quicker, messier way of repairing DNA that can sometimes be necessary for making antibodies during immune responses.
When the researchers introduced mutations into the Shieldin complex—which stop it from forming and protecting broken DNA ends—cells are free to repair DNA via a different method, and this means PARP inhibitors are no longer effective.

***

"'Our study reveals for the first time a complex that is crucial for DNA repair."

Abstract: https://www.nature.com/articles/s41586-018-0340-7

"53BP1 is a chromatin-binding protein that regulates the repair of DNA double-strand breaks by suppressing the nucleolytic resection of DNA termini1,2. This function of 53BP1 requires interactions with PTIP3 and RIF14,5,6,7,8,9, the latter of which recruits REV7 (also known as MAD2L2) to break sites10,11. How 53BP1-pathway proteins shield DNA ends is currently unknown, but there are two models that provide the best potential explanation of their action. In one model the 53BP1 complex strengthens the nucleosomal barrier to end-resection nucleases12,13, and in the other 53BP1 recruits effector proteins with end-protection activity. Here we identify a 53BP1 effector complex, shieldin, that includes C20orf196 (also known as SHLD1), FAM35A (SHLD2), CTC-534A2.2 (SHLD3) and REV7. Shieldin localizes to double-strand-break sites in a 53BP1- and RIF1-dependent manner, and its SHLD2 subunit binds to single-stranded DNA via OB-fold domains that are analogous to those of RPA1 and POT1. Loss of shieldin impairs non-homologous end-joining, leads to defective immunoglobulin class switching and causes hyper-resection. Mutations in genes that encode shieldin subunits also cause resistance to poly(ADP-ribose) polymerase inhibition in BRCA1-deficient cells and tumours, owing to restoration of homologous recombination. Finally, we show that binding of single-stranded DNA by SHLD2 is critical for shieldin function, consistent with a model in which shieldin protects DNA ends to mediate 53BP1-dependent DNA repair."

David Comment: Sorry there is no diagram. This is a very complex system of various proteins which had to be designed when DNA was designed. DNA repair is crucial for the survival of life. That there is more than one system indicates how important repair is.

The simple fact that it CAN be repaired, and IS repaired is enough to explicitly indicate design, from a purely informational level. Randomness doesn't repair or protect itself.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: a new DNA repair mechanism found

by David Turell @, Thursday, July 19, 2018, 18:16 (2080 days ago) @ Balance_Maintained

David Comment: Sorry there is no diagram. This is a very complex system of various proteins which had to be designed when DNA was designed. DNA repair is crucial for the survival of life. That there is more than one system indicates how important repair is.


Tony: The simple fact that it CAN be repaired, and IS repaired is enough to explicitly indicate design, from a purely informational level. Randomness doesn't repair or protect itself.

Designing the repair system along with the code itself is proof that a planning mind and forethought were present to do it.

Genome complexity: retrotransposons in egg production

by David Turell @, Thursday, July 26, 2018, 20:58 (2073 days ago) @ David Turell

Retrotransposons are used to control egg production:

https://phys.org/news/2018-07-genes-disease-evolution.html

"To address this problem, a team of Carnegie researchers developed new techniques to track the mobilization of jumping genes. They found that during a particular period of egg development, a group of jumping-genes called retrotransposons hijacks special cells called nurse cells that nurture the developing eggs. These jumping genes use nurse cells to produce invasive material (copies of themselves called virus-like particles) that move into a nearby egg and then mobilize into the egg's DNA.

***

"The Carnegie team developed approaches to track the movements of jumping genes using the fruit fly Drosophila melanogaster. To facilitate their investigation, they disrupted piRNA suppression to increase the activity of these jumping genes and then monitored the movement of them during the egg-development process. This led to their discovery on the tactic that allows jumping genes to move.

"Carnegie co-author Zhao Zhang explained: "We were very surprised that the these jumping genes barely moved in stem cells that produce developing egg cells, possibly because the stem cells would only have two copies of the genome for these jumping genes to use. Instead, these moving elements used the supporting nurse cells, which could provide up to thousands copies of the genome per cell, as factories to massively manufacture virus-like particles capable of integration. However, they didn't integrate into nurse cells where they were produced.
Rather, they waited while they were transported into an interconnected egg cell, and then added hundreds, if not thousands, of new copies of themselves into the egg DNA. Our research shows how parasitic genetic elements can time their activity and distinguish between different cell types to robustly propagate to drive evolutionary change and cause disease."

"'My group has found that egg development in mammals uses many of the same mechanisms as in the fruit fly, such as feeding the developing egg using nurse cells. So the Zhang group's findings are likely to be important for understanding mammalian evolution and disease as well," commented Allan Spradling, who is a pioneer researcher on studying the egg development in both fruit fly and mammals and a longtime scientist at Carnegie's Department of Embryology."

Comment: Another layer of complexity in the process of reproduction. Hard to imagined this developed by chance.

Genome complexity: copy accuracy controls

by David Turell @, Wednesday, August 15, 2018, 22:09 (2053 days ago) @ David Turell

Extremely precise:

https://peerj.com/articles/4825/

"Abstract


"Statistical and biochemical studies of the standard genetic code (SGC) have found evidence that the impact of mistranslations is minimized in a way that erroneous codes are either synonymous or code for an amino acid with similar polarity as the originally coded amino acid. It could be quantified that the SGC is optimized to protect this specific chemical property as good as possible. In recent work, it has been speculated that the multilevel optimization of the genetic code stands in the wider context of overlapping codes. This work tries to follow the systematic approach on mistranslations and to extend those analyses to the general effect of frameshift mutations on the polarity conservation of amino acids. We generated one million random codes and compared their average polarity change over all triplets and the whole set of possible frameshift mutations. While the natural code—just as for the point mutations—appears to be competitively robust against frameshift mutations as well, we found that both optimizations appear to be independent of each other. For both, better codes can be found, but it becomes significantly more difficult to find candidates that optimize all of these features—just like the SGC does. We conclude that the SGC is not only very efficient in minimizing the consequences of mistranslations, but rather optimized in amino acid polarity conservation for all three effects of code alteration, namely translational errors, point and frameshift mutations. In other words, our result demonstrates that the SGC appears to be much more than just “one in a million”."

The researchers conclude:

"For all three deleterious mechanisms, the genetic code shows clear evidence of its capability to minimize their effects by conserving the polarity of the coded amino acids. The results show that the SGC is most efficient in minimizing the effect of translational errors. It outperforms more than 99.99% of one million randomly generated codes. This effect even got stronger for the combination of all three proposed measures, indicating that all three factors might have been contributed independently to the evolution of this sophisticated, robust, and universal coding. … Thus, our principal conclusion is that stability against frameshift mutations should be put on to the list of the series of features the SGC achieved in the course of evolution."

Comment: These protections were present at life's origin with DNA present. Otherwise it would not have survived. It could not have 'evolved' over time.

Genome complexity: copy accuracy controls

by David Turell @, Thursday, August 16, 2018, 19:27 (2052 days ago) @ David Turell

The molecules that control cell memory in cell division are found:

https://phys.org/news/2018-08-scientists-technology-key-puzzle-cellular.html

"Cells divide constantly throughout life. But how do cells remember whether to develop into skin, liver or intestinal cells? It's a question that has puzzled scientists for many years. Now, scientists from the Faculty of Health and Medical Sciences and the Faculty of Sciences at the University of Copenhagen have come a little closer to understanding this process.

"They have developed a technique that gives new insight into epigenetic cellular memory. With the new technique, called SCAR-seq, the researchers have been able to address how epigenetic information stored in histone proteins is transmitted when DNA is copied and cells divide.

***

"Inside the human cell, our DNA is wrapped around histone proteins. Together, they form a structure called chromatin. When a cell divides, it is crucial that both the DNA and the entire chromatin structure are copied accurately. Chromatin stores epigenetic information that affects which genes are to be expressed. That is, the epigenetic information in our cells helps to control which genes are "turned on" and "off."

"In the new study, the researchers have studied embryonic stem cells from mice. With SCAR-seq, it has become possible for the researchers to identify a protein that is responsible for transfer of histone proteins from the old DNA strand to the two new DNA strands during replication—namely MCM2.

***

"'It has been a recurring question whether the transfer of histones with their chemical modifications was completely random during DNA replication. In our study, we show that it is not a random but a highly controlled process. Our data show that the histones have a preference for one DNA strand, the so-called leading strand, but that MCM2 counteracts this bias and ensures that there is almost symmetry between the two new DNA strands, that is, an even distribution of histone-based information."

"'When we disrupted that mechanism, all histone-based information was transferred to one DNA strand, namely the leading strand, and not to the other, lagging strand. This means that this function by MCM2 is essential for the two new DNA strands to receive the same information stored in histones," says co-author of the study Robin Andersson."

Comment: Uncovering teh extreme complexity one layer at a time. Copy protections had to exist at the origin of life. Only design fits.

Genome complexity: copy accuracy controls

by Balance_Maintained @, U.S.A., Friday, August 17, 2018, 01:16 (2052 days ago) @ David Turell

The molecules that control cell memory in cell division are found:

https://phys.org/news/2018-08-scientists-technology-key-puzzle-cellular.html

"Cells divide constantly throughout life. But how do cells remember whether to develop into skin, liver or intestinal cells? It's a question that has puzzled scientists for many years. Now, scientists from the Faculty of Health and Medical Sciences and the Faculty of Sciences at the University of Copenhagen have come a little closer to understanding this process.

"They have developed a technique that gives new insight into epigenetic cellular memory. With the new technique, called SCAR-seq, the researchers have been able to address how epigenetic information stored in histone proteins is transmitted when DNA is copied and cells divide.

***

"Inside the human cell, our DNA is wrapped around histone proteins. Together, they form a structure called chromatin. When a cell divides, it is crucial that both the DNA and the entire chromatin structure are copied accurately. Chromatin stores epigenetic information that affects which genes are to be expressed. That is, the epigenetic information in our cells helps to control which genes are "turned on" and "off."

"In the new study, the researchers have studied embryonic stem cells from mice. With SCAR-seq, it has become possible for the researchers to identify a protein that is responsible for transfer of histone proteins from the old DNA strand to the two new DNA strands during replication—namely MCM2.

***

"'It has been a recurring question whether the transfer of histones with their chemical modifications was completely random during DNA replication. In our study, we show that it is not a random but a highly controlled process. Our data show that the histones have a preference for one DNA strand, the so-called leading strand, but that MCM2 counteracts this bias and ensures that there is almost symmetry between the two new DNA strands, that is, an even distribution of histone-based information."

"'When we disrupted that mechanism, all histone-based information was transferred to one DNA strand, namely the leading strand, and not to the other, lagging strand. This means that this function by MCM2 is essential for the two new DNA strands to receive the same information stored in histones," says co-author of the study Robin Andersson."

David: Comment: Uncovering teh extreme complexity one layer at a time. Copy protections had to exist at the origin of life. Only design fits.

This is predicted by my alternative hypothesis to evolution. For the sake of conversation, I will refer to it as the Living Programming Language.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity: cell wall codes

by David Turell @, Thursday, April 04, 2019, 19:56 (1821 days ago) @ Balance_Maintained

Beyond genome controls are cell wall codes to organize entry of various molecules:

https://www.newscientist.com/article/mg24132230-300-move-over-dna-lifes-other-code-is-m...

"NOT a lot of people know this, but babies are made with a handshake. True, that isn’t all that is involved. Often it starts with two people falling in love. But at some point biology takes over and a sperm must burrow its way into an egg. There is, however, more to the story.

"On reaching the egg, the sperm meets the zona pellucida, a thick jacket of sugars that only sperm cells have the right biochemical tools to grab hold of. That “molecular handshake”, as Kamil Godula at the University of California, San Diego, puts it, is the most crucial step in the process that gets human life started.

"Sugary handshakes aren’t just involved in baby-making. It turns out that every type of cell in our bodies has a unique sugar coating. And whenever anything interacts with a cell, it must recognise that sugar code and use the appropriate secret handshake. It happens when bacteria and viruses infect us, when a growing brain cell feels its way past its neighbours, and when our stem cells receive the marching orders that will define what type of tissue they will develop into.

"Learn to read and write this sugary language, then, and we would have a powerful new way of intervening in cells’ activities to control disease and plenty besides. It won’t be easy. Unlike DNA, this code is fiendishly complex. But we are finally beginning to master the language of our cells."

Comment: The rest of the article is paywall blocked, but you get the idea. It is part of the overall automaticity of living beings.

Genome complexity: how humans correct errors

by David Turell @, Saturday, November 07, 2020, 20:40 (1238 days ago) @ David Turell

An attempt to develop drugs to counteract genome mistakes:

https://phys.org/news/2020-11-two-birds-one-stone-strategy-rna-repeat-expansion-disease...

"A new strategy for treating a variety of diseases known as RNA-repeat expansion disorders, which affect millions of people, has shown promise in proof-of-principle tests conducted by scientists at Scripps Research.

"The results suggest that someday, a handful of well-targeted drugs might be able to treat the more than 40 human disorders—including Huntington's disease and variants of amyotrophic lateral sclerosis (ALS)—that arise from RNA-repeat expansions.

"'This study lays a foundation for the development of drugs that can address multiple repeat-expansion diseases by targeting shared abnormal structures on their RNAs,"

***

"In RNA-repeat expansion diseases, mutant genes contain excess DNA in the form of dozens or even hundreds of repeating short strings of DNA "letters." In cells where these mutant genes are active, that DNA is copied out into RNA molecules on the way to being translated into proteins. The resulting abnormal RNAs can cause trouble in a variety of ways, such as by folding up into structures that are toxic to cells.

"In the study, published in Cell Chemical Biology, the scientists showed that a potential drug molecule they developed can neutralize the toxic RNA that causes two distinct repeat-expansion disorders, myotonic dystrophy 1 (DM1) and Fuchs endothelial corneal dystrophy (FECD). In the latter case, it can do so by an unexpected but powerful mechanism.

***

"These disorders arise from different mutant genes, and consequently appear in different cell types, but involve virtually the same toxic mechanism: In each case, the inclusion of an abnormally long sequence of CUG repeats causes the RNA copied from the gene to form structures that are "sticky" to certain other proteins in the cell, and effectively capture them—preventing them from doing their jobs in the cell. The depletion of one of these captured proteins, MBNL1, is a particularly important cause of cell damage and symptoms in DM1 and FECD.

***

"Targeting toxic RNAs with small organic molecules that can be put into pill form has generally been very challenging, so far, Disney notes, but the finding in this study points to the promising possibility of using such molecules not just to block bad RNAs but to trigger their destruction.

"If a drug causes a toxic RNA to be destroyed instead of merely blocking it, then the effect should be longer lasting," he says.

"Having performed their proof-of-principle demonstration, he and his team, which includes a startup biotech company, Expansion Therapeutics, are continuing to develop the molecule tested in the study as a potential drug treatment for DM1 and FECD.

"The researchers also are taking a similar approach in developing potential drug treatments for RNA repeat-expansion diseases involving CAG repeats, which include the progressive and fatal neurological disorder known as Huntington's disease."

Comment: This study shows how human ingenuity can solve the errors problem. In our country this error rate is .0000000.424%. Not nice for those affected, but a tiny error rate.

Genome complexity: how humans correct errors

by dhw, Sunday, November 08, 2020, 08:41 (1237 days ago) @ David Turell

QUOTES: We need to think about consciousness itself as an archaeologist thinks about layers of sedimentary strata. At the lower layers, we have basic drives that prod us (and other animals) out into the environment for the exploitation of resources. Thirst, lust, fear and so on are triggers in evolutionarily earlier regions of the brain that stimulate vertebrates toward satisfaction and a return to homeostasis (physiological balance).

"It is probably most accurate to say that primary and secondary emotions have phenomenal consciousness (experiential feeling), but lack access consciousness (the ability to rationally access, manipulate and reflect upon emotions).

This is what I mean when I talk of different levels of intelligence/consciousness. But in the context of evolution, the basic drive is not confined to the brain and the exploitation of resources (i.e. finding food) – it also encompasses finding different modes of survival (e.g. avoiding predators, using or building shelters, countering every threat to existence). And I would suggest that this all begins at cellular level, with “phenomenally conscious” cells cooperating over billions of years to form increasingly complex structures, INCLUDING the brain and every other organ we know of and every other life form we know of. This is the “continuum” of evolution that David talks of, as organisms branch out into an ever more variegated bush, with just one of millions of “lines” leading to humans. The cell communities that form the brain itself would have followed precisely the same process of complexification as they responded to new requirements, including control of their new organs. The brains of most life forms would have settled once they had achieved “satisfaction and homeostasis” but, as we know, the human brain continued to expand as “access consciousness” enabled early humans to rationalize and manipulate – not just in terms of reflecting on emotions etc, but also reflecting on and implementing new methods of surviving and/or exploiting their environment.

Genome complexity: how humans correct errors; dhw confusion

by David Turell @, Sunday, November 08, 2020, 17:28 (1237 days ago) @ dhw
edited by David Turell, Sunday, November 08, 2020, 17:39

These quotes are from a totally different entry , but his discussion is appropriate to this entry from yesterday website:

https://aeon.co/essays/human-culture-and-cognition-evolved-through-the-emotions?utm_sou...

QUOTES: We need to think about consciousness itself as an archaeologist thinks about layers of sedimentary strata. At the lower layers, we have basic drives that prod us (and other animals) out into the environment for the exploitation of resources. Thirst, lust, fear and so on are triggers in evolutionarily earlier regions of the brain that stimulate vertebrates toward satisfaction and a return to homeostasis (physiological balance).

"It is probably most accurate to say that primary and secondary emotions have phenomenal consciousness (experiential feeling), but lack access consciousness (the ability to rationally access, manipulate and reflect upon emotions).

dhw: This is what I mean when I talk of different levels of intelligence/consciousness. But in the context of evolution, the basic drive is not confined to the brain and the exploitation of resources (i.e. finding food) – it also encompasses finding different modes of survival (e.g. avoiding predators, using or building shelters, countering every threat to existence). And I would suggest that this all begins at cellular level, with “phenomenally conscious” cells cooperating over billions of years to form increasingly complex structures, INCLUDING the brain and every other organ we know of and every other life form we know of. This is the “continuum” of evolution that David talks of, as organisms branch out into an ever more variegated bush, with just one of millions of “lines” leading to humans. The cell communities that form the brain itself would have followed precisely the same process of complexification as they responded to new requirements, including control of their new organs. The brains of most life forms would have settled once they had achieved “satisfaction and homeostasis” but, as we know, the human brain continued to expand as “access consciousness” enabled early humans to rationalize and manipulate – not just in terms of reflecting on emotions etc, but also reflecting on and implementing new methods of surviving and/or exploiting their environment.

dhw is correct: Every branch of the bush reached satisfactory level of survival ability and stopped evolving. I have constantly pointed out apes did just fine until we overran the world and pushed them aside into small survival areas. This brings back my philosophic point: why did a single branch push forward and enlarge their brain? Darwin survival theory offers no significant answer. The earliest ape/hominin transitional forms COULD NOT have any foresight of what their cells needed to develop to achieve what we have now. This is one major reason I left agnosticism. Some agent drove this. Further, my lifelong knowledge and study of biochemistry easily recognized the degree of complexity that requires design of the systems. Acceptance of a designing God is the only reasonable answer. The key is full understanding of the extreme biochemical complexity, which could not appear by chance.

Genome complexity: how humans correct errors; dhw confusion

by dhw, Monday, November 09, 2020, 10:50 (1236 days ago) @ David Turell

DAVID: These quotes are from a totally different entry , but his discussion is appropriate to this entry from yesterday website:
https://aeon.co/essays/human-culture-and-cognition-evolved-through-the-emotions?utm_sou...

QUOTES: We need to think about consciousness itself as an archaeologist thinks about layers of sedimentary strata. At the lower layers, we have basic drives that prod us (and other animals) out into the environment for the exploitation of resources. Thirst, lust, fear and so on are triggers in evolutionarily earlier regions of the brain that stimulate vertebrates toward satisfaction and a return to homeostasis (physiological balance).

"It is probably most accurate to say that primary and secondary emotions have phenomenal consciousness (experiential feeling), but lack access consciousness (the ability to rationally access, manipulate and reflect upon emotions).

dhw: This is what I mean when I talk of different levels of intelligence/consciousness. But in the context of evolution, the basic drive is not confined to the brain and the exploitation of resources (i.e. finding food) – it also encompasses finding different modes of survival (e.g. avoiding predators, using or building shelters, countering every threat to existence). And I would suggest that this all begins at cellular level, with “phenomenally conscious” cells cooperating over billions of years to form increasingly complex structures, INCLUDING the brain and every other organ we know of and every other life form we know of. This is the “continuum” of evolution that David talks of, as organisms branch out into an ever more variegated bush, with just one of millions of “lines” leading to humans. The cell communities that form the brain itself would have followed precisely the same process of complexification as they responded to new requirements, including control of their new organs. The brains of most life forms would have settled once they had achieved “satisfaction and homeostasis” but, as we know, the human brain continued to expand as “access consciousness” enabled early humans to rationalize and manipulate – not just in terms of reflecting on emotions etc, but also reflecting on and implementing new methods of surviving and/or exploiting their environment.

DAVID: dhw is correct: Every branch of the bush reached satisfactory level of survival ability and stopped evolving. I have constantly pointed out apes did just fine until we overran the world and pushed them aside into small survival areas. This brings back my philosophic point: why did a single branch push forward and enlarge their brain? Darwin survival theory offers no significant answer.

Nobody knows how we acquired our extra degrees of consciousness – and nobody knows how consciousness arose in the first place. That is why we have so many different theories.

DAVID: The earliest ape/hominin transitional forms COULD NOT have any foresight of what their cells needed to develop to achieve what we have now.

This is a major difference between us. What I propose does not require one iota of foresight. My proposal, as you well know, is that every advance was made IN RESPONSE TO new requirements – not in anticipation of them. One simple example: you tell us your God turned pre-whale legs into fins before the pre-whale entered the water. To me it seems sheer common sense that fins would have resulted from adaptation to life in the water, once the pre-whale discovered that the marine environment was more favourable for its survival.

DAVID: This is one major reason I left agnosticism. Some agent drove this. Further, my lifelong knowledge and study of biochemistry easily recognized the degree of complexity that requires design of the systems. Acceptance of a designing God is the only reasonable answer. The key is full understanding of the extreme biochemical complexity, which could not appear by chance.

Over and over again, I have agreed with you that the extreme biochemical complexity provides the best possible evidence for design, but the theory I have proposed above promotes the design theory and does not preclude the existence of a designer God! You know perfectly well that it allows for God as the designer of the intelligent cell, and there is no mention of chance as the designer of the complexities. Now perhaps you will point out which aspects of my theory are confused.

Genome complexity: how humans correct errors; dhw confusion

by David Turell @, Monday, November 09, 2020, 14:45 (1236 days ago) @ dhw

DAVID: These quotes are from a totally different entry , but his discussion is appropriate to this entry from yesterday website:
https://aeon.co/essays/human-culture-and-cognition-evolved-through-the-emotions?utm_sou...

QUOTES: We need to think about consciousness itself as an archaeologist thinks about layers of sedimentary strata. At the lower layers, we have basic drives that prod us (and other animals) out into the environment for the exploitation of resources. Thirst, lust, fear and so on are triggers in evolutionarily earlier regions of the brain that stimulate vertebrates toward satisfaction and a return to homeostasis (physiological balance).

"It is probably most accurate to say that primary and secondary emotions have phenomenal consciousness (experiential feeling), but lack access consciousness (the ability to rationally access, manipulate and reflect upon emotions).

dhw: This is what I mean when I talk of different levels of intelligence/consciousness. But in the context of evolution, the basic drive is not confined to the brain and the exploitation of resources (i.e. finding food) – it also encompasses finding different modes of survival (e.g. avoiding predators, using or building shelters, countering every threat to existence). And I would suggest that this all begins at cellular level, with “phenomenally conscious” cells cooperating over billions of years to form increasingly complex structures, INCLUDING the brain and every other organ we know of and every other life form we know of. This is the “continuum” of evolution that David talks of, as organisms branch out into an ever more variegated bush, with just one of millions of “lines” leading to humans. The cell communities that form the brain itself would have followed precisely the same process of complexification as they responded to new requirements, including control of their new organs. The brains of most life forms would have settled once they had achieved “satisfaction and homeostasis” but, as we know, the human brain continued to expand as “access consciousness” enabled early humans to rationalize and manipulate – not just in terms of reflecting on emotions etc, but also reflecting on and implementing new methods of surviving and/or exploiting their environment.

DAVID: dhw is correct: Every branch of the bush reached satisfactory level of survival ability and stopped evolving. I have constantly pointed out apes did just fine until we overran the world and pushed them aside into small survival areas. This brings back my philosophic point: why did a single branch push forward and enlarge their brain? Darwin survival theory offers no significant answer.

dhw: Nobody knows how we acquired our extra degrees of consciousness – and nobody knows how consciousness arose in the first place. That is why we have so many different theories.

DAVID: The earliest ape/hominin transitional forms COULD NOT have any foresight of what their cells needed to develop to achieve what we have now.

dhw: This is a major difference between us. What I propose does not require one iota of foresight. My proposal, as you well know, is that every advance was made IN RESPONSE TO new requirements – not in anticipation of them. One simple example: you tell us your God turned pre-whale legs into fins before the pre-whale entered the water. To me it seems sheer common sense that fins would have resulted from adaptation to life in the water, once the pre-whale discovered that the marine environment was more favourable for its survival.

'Sheer common sense' offers no facts. Hippos lived in water since forever with no change!


DAVID: This is one major reason I left agnosticism. Some agent drove this. Further, my lifelong knowledge and study of biochemistry easily recognized the degree of complexity that requires design of the systems. Acceptance of a designing God is the only reasonable answer. The key is full understanding of the extreme biochemical complexity, which could not appear by chance.

dhw: Over and over again, I have agreed with you that the extreme biochemical complexity provides the best possible evidence for design, but the theory I have proposed above promotes the design theory and does not preclude the existence of a designer God! You know perfectly well that it allows for God as the designer of the intelligent cell, and there is no mention of chance as the designer of the complexities. Now perhaps you will point out which aspects of my theory are confused.

The requirement of design requires the ability of seeing the future needs and designing for them. None of what is seen in biochemical complexity can do this bit by bit, but only all at once with supreme coordination of all processes. You are asking cells to be God. Not for me. All cells show now, even Shapiros bacteria, is proper responses to important stimuli. Present state only, nothing futuristic.

Genome complexity: how humans correct errors; dhw confusion

by dhw, Tuesday, November 10, 2020, 11:16 (1235 days ago) @ David Turell

dhw: This is a major difference between us. What I propose does not require one iota of foresight. My proposal, as you well know, is that every advance was made IN RESPONSE TO new requirements – not in anticipation of them. One simple example: you tell us your God turned pre-whale legs into fins before the pre-whale entered the water. To me it seems sheer common sense that fins would have resulted from adaptation to life in the water, once the pre-whale discovered that the marine environment was more favourable for its survival.

DAVID: 'Sheer common sense' offers no facts. Hippos lived in water since forever with no change!

Their survival shows that they did not need to change. How does that prove that your God changed legs to fins before pre-whales entered the water?

DAVID: […] my lifelong knowledge and study of biochemistry easily recognized the degree of complexity that requires design of the systems. Acceptance of a designing God is the only reasonable answer. The key is full understanding of the extreme biochemical complexity, which could not appear by chance.

dhw: Over and over again, I have agreed with you that the extreme biochemical complexity provides the best possible evidence for design, but the theory I have proposed above promotes the design theory and does not preclude the existence of a designer God! You know perfectly well that it allows for God as the designer of the intelligent cell, and there is no mention of chance as the designer of the complexities. Now perhaps you will point out which aspects of my theory are confused.

DAVID: The requirement of design requires the ability of seeing the future needs and designing for them.

That may be so if you are thinking in terms of human preparations for the future, but we are talking here about the difference between chance and deliberate, purposeful activity as the cause of organisms adapting to or exploiting the conditions in which they find themselves. We do not know the cause of evolutionary innovation, but we certainly know the cause of adaptation, which is that new conditions trigger changes in the organism – as opposed to organisms changing in advance of new conditions. These changes are a deliberate, purposeful activity, and so it is perfectly feasible that the mechanism enabling them would also have enabled the major changes required for speciation. The borderline between adaptation and innovation is not clear anyway, as is evident from the whale example.

DAVID: None of what is seen in biochemical complexity can do this bit by bit, but only all at once with supreme coordination of all processes. You are asking cells to be God. Not for me. All cells show now, even Shapiros bacteria, is proper responses to important stimuli. Present state only, nothing futuristic.

Precisely. Nobody has ever seen an organism change itself in preparation for the future. And of course the cell communities must coordinate in every process. But I am not asking cells to be God! As you know perfectly well, my proposal encompasses the possibility of God as designer of the intelligent cell. I am always surprised that you refuse to consider your God capable of designing a mechanism to produce all the billions of changes you make him preprogramme 3.8 billion years ago, or keep personally dabbling one by one.

Under “Human evolution”:

"These adaptations are believed to have taken place during a period of environmental change, when climate records indicate that the region was drying out. The increasingly arid conditions led to the extinction of several mammal species and may have placed hominins under dietary stress."

DAVID: This adds to the story and tells us that many different types of hominins coexisted, as more advanced forms developed, and also notes the forms modified as needs changed. Was this epigenetics in action, but not speciation. since it appears within the same species?

Yes, forms modify in response to new needs ("as needs changed"). That is the only process we know of. Since we both believe in common descent, every stage in the line from bacteria to humans would have entailed some form of modification. This can hardly be said to fit in with your theory that your God preprogrammed or dabbled every change in anticipation of future needs.

Genome complexity: how humans correct errors; dhw confusion

by David Turell @, Tuesday, November 10, 2020, 18:11 (1235 days ago) @ dhw

dhw: This is a major difference between us. What I propose does not require one iota of foresight. My proposal, as you well know, is that every advance was made IN RESPONSE TO new requirements – not in anticipation of them. One simple example: you tell us your God turned pre-whale legs into fins before the pre-whale entered the water. To me it seems sheer common sense that fins would have resulted from adaptation to life in the water, once the pre-whale discovered that the marine environment was more favourable for its survival.

DAVID: 'Sheer common sense' offers no facts. Hippos lived in water since forever with no change!

dhw: Their survival shows that they did not need to change. How does that prove that your God changed legs to fins before pre-whales entered the water?

It is my common sense interpretation.


DAVID: The requirement of design requires the ability of seeing the future needs and designing for them.

dhw: That may be so if you are thinking in terms of human preparations for the future, but we are talking here about the difference between chance and deliberate, purposeful activity as the cause of organisms adapting to or exploiting the conditions in which they find themselves. We do not know the cause of evolutionary innovation, but we certainly know the cause of adaptation, which is that new conditions trigger changes in the organism – as opposed to organisms changing in advance of new conditions. These changes are a deliberate, purposeful activity, and so it is perfectly feasible that the mechanism enabling them would also have enabled the major changes required for speciation. The borderline between adaptation and innovation is not clear anyway, as is evident from the whale example.

The bold is an excellent analysis of our problem. The gap we have to cross is there is no physical evidence in the fossil record of small necessary adaptations leading to new species. So the big gaps create the unsolved problem.


DAVID: None of what is seen in biochemical complexity can do this bit by bit, but only all at once with supreme coordination of all processes. You are asking cells to be God. Not for me. All cells show now, even Shapiros bacteria, is proper responses to important stimuli. Present state only, nothing futuristic.

dhw: Precisely. Nobody has ever seen an organism change itself in preparation for the future. And of course the cell communities must coordinate in every process. But I am not asking cells to be God! As you know perfectly well, my proposal encompasses the possibility of God as designer of the intelligent cell. I am always surprised that you refuse to consider your God capable of designing a mechanism to produce all the billions of changes you make him preprogramme 3.8 billion years ago, or keep personally dabbling one by one.

My reasoning is designing a mechanism to design for the future makes control one step away from the first designer, introducing possible errors.


Under “Human evolution”:

"These adaptations are believed to have taken place during a period of environmental change, when climate records indicate that the region was drying out. The increasingly arid conditions led to the extinction of several mammal species and may have placed hominins under dietary stress."

DAVID: This adds to the story and tells us that many different types of hominins coexisted, as more advanced forms developed, and also notes the forms modified as needs changed. Was this epigenetics in action, but not speciation. since it appears within the same species?

dhw: Yes, forms modify in response to new needs ("as needs changed"). That is the only process we know of. Since we both believe in common descent, every stage in the line from bacteria to humans would have entailed some form of modification. This can hardly be said to fit in with your theory that your God preprogrammed or dabbled every change in anticipation of future needs.

Of course it fits if God is responsible to do all designs of advances.

Genome complexity: how humans correct errors; dhw confusion

by dhw, Wednesday, November 11, 2020, 10:54 (1234 days ago) @ David Turell

dhw: This is a major difference between us. What I propose does not require one iota of foresight. My proposal, as you well know, is that every advance was made IN RESPONSE TO new requirements – not in anticipation of them. One simple example: you tell us your God turned pre-whale legs into fins before the pre-whale entered the water. To me it seems sheer common sense that fins would have resulted from adaptation to life in the water, once the pre-whale discovered that the marine environment was more favourable for its survival.

DAVID: 'Sheer common sense' offers no facts. Hippos lived in water since forever with no change!

dhw: Their survival shows that they did not need to change. How does that prove that your God changed legs to fins before pre-whales entered the water?

DAVID: It is my common sense interpretation.

So common sense tells you that 3.8 billion years ago your God would have preprogrammed the first cells not only to develop pre-whales (not to mention the brontosaurus and H. sapiens and millions of other life forms)) out of bacteria, but also to change pre-whale legs to fins when the time came for them to enter the water. Alternatively, he stepped in to perform an operation on a group of pre-whales, and then told them to enter the water. And yet amazingly, even today we see some life forms changing themselves IN RESPONSE to new conditions, and nobody has ever seen such changes take place BEFORE conditions have changed.

dhw: These changes are a deliberate, purposeful activity, and so it is perfectly feasible that the mechanism enabling them would also have enabled the major changes required for speciation. The borderline between adaptation and innovation is not clear anyway, as is evident from the whale example.

DAVID: The bold is an excellent analysis of our problem. The gap we have to cross is there is no physical evidence in the fossil record of small necessary adaptations leading to new species. So the big gaps create the unsolved problem.

Correct. And that is why we come up with our different theories. Then we test them to see if they make sense. I'm afraid the idea of pre-whales waking up one morning to find their legs have turned into fins elicits more of a giggle than a nod from me.

dhw: I am always surprised that you refuse to consider your God capable of designing a mechanism to produce all the billions of changes you make him preprogramme 3.8 billion years ago, or keep personally dabbling one by one.

DAVID: My reasoning is designing a mechanism to design for the future makes control one step away from the first designer, introducing possible errors.

According to you, your God’s design introduced errors anyway. We have a whole thread devoted to that subject, and the problem with your “control” theory is dealt with on that thread (which has broadened out again into a discussion of your whole theory of evolution). But you are right – my theory (theistic version) has God deliberately sacrificing control, and I offer a logical reason for his doing so under “Theodicy”.

Genome complexity: how humans correct errors; dhw confusion

by David Turell @, Wednesday, November 11, 2020, 15:32 (1234 days ago) @ dhw

dhw: This is a major difference between us. What I propose does not require one iota of foresight. My proposal, as you well know, is that every advance was made IN RESPONSE TO new requirements – not in anticipation of them. One simple example: you tell us your God turned pre-whale legs into fins before the pre-whale entered the water. To me it seems sheer common sense that fins would have resulted from adaptation to life in the water, once the pre-whale discovered that the marine environment was more favourable for its survival.

DAVID: 'Sheer common sense' offers no facts. Hippos lived in water since forever with no change!

dhw: Their survival shows that they did not need to change. How does that prove that your God changed legs to fins before pre-whales entered the water?

DAVID: It is my common sense interpretation.

dhw: So common sense tells you that 3.8 billion years ago your God would have preprogrammed the first cells not only to develop pre-whales (not to mention the brontosaurus and H. sapiens and millions of other life forms)) out of bacteria, but also to change pre-whale legs to fins when the time came for them to enter the water. Alternatively, he stepped in to perform an operation on a group of pre-whales, and then told them to enter the water. And yet amazingly, even today we see some life forms changing themselves IN RESPONSE to new conditions, and nobody has ever seen such changes take place BEFORE conditions have changed.

Again your mishmash trying to compare simple adaptations within species to speciation. I don't know how God created species, pre-programming or dabbling or whatever. All I do know is design by a designing mind is required.


dhw: These changes are a deliberate, purposeful activity, and so it is perfectly feasible that the mechanism enabling them would also have enabled the major changes required for speciation. The borderline between adaptation and innovation is not clear anyway, as is evident from the whale example.

DAVID: The bold is an excellent analysis of our problem. The gap we have to cross is there is no physical evidence in the fossil record of small necessary adaptations leading to new species. So the big gaps create the unsolved problem.

dhw: Correct. And that is why we come up with our different theories. Then we test them to see if they make sense. I'm afraid the idea of pre-whales waking up one morning to find their legs have turned into fins elicits more of a giggle than a nod from me.

I agree, but the giggle has to explain the fossil record gaps.


dhw: I am always surprised that you refuse to consider your God capable of designing a mechanism to produce all the billions of changes you make him preprogramme 3.8 billion years ago, or keep personally dabbling one by one.

DAVID: My reasoning is designing a mechanism to design for the future makes control one step away from the first designer, introducing possible errors.

dhw: According to you, your God’s design introduced errors anyway. We have a whole thread devoted to that subject, and the problem with your “control” theory is dealt with on that thread (which has broadened out again into a discussion of your whole theory of evolution). But you are right – my theory (theistic version) has God deliberately sacrificing control, and I offer a logical reason for his doing so under “Theodicy”.

I don't view your theory in theodicy as logical based on my view of God in control

Genome complexity: how humans correct errors; dhw confusion

by dhw, Thursday, November 12, 2020, 12:12 (1233 days ago) @ David Turell

dhw: … even today we see some life forms changing themselves IN RESPONSE to new conditions, and nobody has ever seen such changes take place BEFORE conditions have changed.

DAVID: Again your mishmash trying to compare simple adaptations within species to speciation. I don't know how God created species, pre-programming or dabbling or whatever. All I do know is design by a designing mind is required.

I am not comparing them. I am pointing out that we KNOW organisms change their structures IN RESPONSE to new conditions. I don’t know what your “whatever” can refer to, since you have only ever offered us the two methods, and you have only ever argued that evolutionary innovations take place BEFORE the new conditions for which they are used. I am not objecting to the case for design, which is covered by my cellular intelligence theory, which in turn leaves open the possibility of your God as designer of cellular intelligence.

dhw: I'm afraid the idea of pre-whales waking up one morning to find their legs have turned into fins elicits more of a giggle than a nod from me.

DAVID: I agree, but the giggle has to explain the fossil record gaps.

Firstly, every major fossil find is a sensation, because preservation over millions and millions of years is so unlikely, and secondly, if your God can restructure cell communities, why do you think he is incapable of designing cell communities to do the same thing – especially since we know there is such a mechanism for restructuring without his intervention (i.e. adaptation).

dhw: I am always surprised that you refuse to consider your God capable of designing a mechanism to produce all the billions of changes you make him preprogramme 3.8 billion years ago, or keep personally dabbling one by one.

DAVID: My reasoning is designing a mechanism to design for the future makes control one step away from the first designer, introducing possible errors.

dhw: According to you, your God’s design introduced errors anyway. We have a whole thread devoted to that subject, and the problem with your “control” theory is dealt with on that thread (which has broadened out again into a discussion of your whole theory of evolution). [Your "design for the future" theory was dealt with on this thread.] But you are right – my theory (theistic version) has God deliberately sacrificing control, and I offer a logical reason for his doing so under “Theodicy”.

DAVID: I don't view your theory in theodicy as logical based on my view of God in control.

You are simply saying that my theory is illogical because it differs from your theory! My idea that your God did not WANT control is no more and no less feasible than your idea that he did. Nothing to do with logic. Your theory leads you to admitting that you have no idea why he would have created bad bugs. You call that logic. My theory explains logically how the bad bugs could have come into existence, and why your God allowed them to do so, and it also explains the vast variety of life forms and natural wonders which have/had nothing to do with humans.

Genome complexity: how humans correct errors; dhw confusion

by David Turell @, Thursday, November 12, 2020, 17:34 (1233 days ago) @ dhw

dhw: … even today we see some life forms changing themselves IN RESPONSE to new conditions, and nobody has ever seen such changes take place BEFORE conditions have changed.

DAVID: Again your mishmash trying to compare simple adaptations within species to speciation. I don't know how God created species, pre-programming or dabbling or whatever. All I do know is design by a designing mind is required.

I am not comparing them. I am pointing out that we KNOW organisms change their structures IN RESPONSE to new conditions. I don’t know what your “whatever” can refer to, since you have only ever offered us the two methods, and you have only ever argued that evolutionary innovations take place BEFORE the new conditions for which they are used. I am not objecting to the case for design, which is covered by my cellular intelligence theory, which in turn leaves open the possibility of your God as designer of cellular intelligence.

What major structures change in species adaptation? Nothing major we know of. Yes we also differ about design. Logically God must directly design, rather than putting it off to a secondary independent mechanism by cells.


dhw: I'm afraid the idea of pre-whales waking up one morning to find their legs have turned into fins elicits more of a giggle than a nod from me.

DAVID: I agree, but the giggle has to explain the fossil record gaps.

dhw: Firstly, every major fossil find is a sensation, because preservation over millions and millions of years is so unlikely, and secondly, if your God can restructure cell communities, why do you think he is incapable of designing cell communities to do the same thing – especially since we know there is such a mechanism for restructuring without his intervention (i.e. adaptation).

All quite minor. Again extrapolating to major change in design.


dhw: I am always surprised that you refuse to consider your God capable of designing a mechanism to produce all the billions of changes you make him preprogramme 3.8 billion years ago, or keep personally dabbling one by one.

DAVID: My reasoning is designing a mechanism to design for the future makes control one step away from the first designer, introducing possible errors.

dhw: According to you, your God’s design introduced errors anyway. We have a whole thread devoted to that subject, and the problem with your “control” theory is dealt with on that thread (which has broadened out again into a discussion of your whole theory of evolution). [Your "design for the future" theory was dealt with on this thread.] But you are right – my theory (theistic version) has God deliberately sacrificing control, and I offer a logical reason for his doing so under “Theodicy”.

DAVID: I don't view your theory in theodicy as logical based on my view of God in control.

dhw: You are simply saying that my theory is illogical because it differs from your theory! My idea that your God did not WANT control is no more and no less feasible than your idea that he did. Nothing to do with logic. Your theory leads you to admitting that you have no idea why he would have created bad bugs. You call that logic. My theory explains logically how the bad bugs could have come into existence, and why your God allowed them to do so, and it also explains the vast variety of life forms and natural wonders which have/had nothing to do with humans.

Each theory has a background of facts to be considered. Our considerations differ. My view of Godadn his intentions are not yours.

Genome complexity: how humans correct errors; dhw confusion

by dhw, Friday, November 13, 2020, 07:13 (1232 days ago) @ David Turell

dhw: ...we KNOW organisms change their structures IN RESPONSE to new conditions.

DAVID: What major structures change in species adaptation? Nothing major we know of. Yes we also differ about design. Logically God must directly design, rather than putting it off to a secondary independent mechanism by cells.

It’s difficult to distinguish between adaptation and innovation when we consider all the different changes from land-based pre-whale life to marine life. And I have absolutely no idea why a divine 3.8-billion-year-old programme for every single life form, econiche, strategy and natural wonder in the history of life on Earth, or a vast number of individual operations on legs and brains and pelvises, and lectures delivered on nest-building etc., should be regarded as more “logical” than the invention of an intelligent mechanism capable of doing its own designing.

I remain baffled by your reference to “dhw confusion” in the heading of this thread. What do you find confusing about the concept of cellular intelligence as the driver of evolution, compared to the labyrinthine theory of divine programmes and dabbles and every life form with no connection to humans being part of the direct design of humans? Meanwhile, thank you for two more articles which fit in neatly with the concept of bacterial and cellular intelligence:

DAVID: (under “DNA fights off viruses”) Bacteria edit their DNA to self-destruct and save the colony. I would ask how did this developed? Did bacteria learn this on their own or did it happen by design?

They seem to behave just like ants. And yes, I would suggest that just like ants, they design and pass on different ways of surviving different threats.

Under: "Sensory neurons do more than accept":
QUOTE: "The findings suggest that the sensory cortex is not just sensory, as previously thought. Instead of responding only to stimuli around us, Dr. Maravall's study suggests that the sensory neurons are also involved in processing the meaning of the stimuli, and planning the subsequent behavioural responses."

Wow, we have cells processing information and planning what to do with it. Sounds like intelligence to me.

Genome complexity: how humans correct errors; dhw confusion

by David Turell @, Friday, November 13, 2020, 23:02 (1232 days ago) @ dhw

dhw: ...we KNOW organisms change their structures IN RESPONSE to new conditions.

DAVID: What major structures change in species adaptation? Nothing major we know of. Yes we also differ about design. Logically God must directly design, rather than putting it off to a secondary independent mechanism by cells.

dhw: It’s difficult to distinguish between adaptation and innovation when we consider all the different changes from land-based pre-whale life to marine life. And I have absolutely no idea why a divine 3.8-billion-year-old programme for every single life form, econiche, strategy and natural wonder in the history of life on Earth, or a vast number of individual operations on legs and brains and pelvises, and lectures delivered on nest-building etc., should be regarded as more “logical” than the invention of an intelligent mechanism capable of doing its own designing.

It is an issue of direct control or second-hand control, and how views a purposeful God.


dhw: I remain baffled by your reference to “dhw confusion” in the heading of this thread.

Go back in recent history and fix your memory. You put the wrong answer under the this heading:

Genome complexity: how humans correct errors - dhw, 2020-11-08, 08:41


DAVID: (under “DNA fights off viruses”) Bacteria edit their DNA to self-destruct and save the colony. I would ask how did this developed? Did bacteria learn this on their own or did it happen by design?

dhw: They seem to behave just like ants. And yes, I would suggest that just like ants, they design and pass on different ways of surviving different threats.

Under: "Sensory neurons do more than accept":
QUOTE: "The findings suggest that the sensory cortex is not just sensory, as previously thought. Instead of responding only to stimuli around us, Dr. Maravall's study suggests that the sensory neurons are also involved in processing the meaning of the stimuli, and planning the subsequent behavioural responses."

dhw: Wow, we have cells processing information and planning what to do with it. Sounds like intelligence to me.

Why not? God designed them that way.

Genome complexity: how humans correct errors; dhw confusion

by dhw, Saturday, November 14, 2020, 11:45 (1231 days ago) @ David Turell

dhw: I have absolutely no idea why a divine 3.8-billion-year-old programme for every single life form, econiche, strategy and natural wonder in the history of life on Earth, or a vast number of individual operations on legs and brains and pelvises, and lectures delivered on nest-building etc., should be regarded as more “logical” than the invention of an intelligent mechanism capable of doing its own designing.

DAVID: It is an issue of direct control or second-hand control, and how views a purposeful God.

Agreed. How does that make direct control more “logical” than allowing organisms to do their own designing, especially if you claim that your controlling God’s goal was to directly design humans, and he did this by directly designing millions of branches of life that had no connection with humans.

dhw: I remain baffled by your reference to “dhw confusion” in the heading of this thread.

DAVID: Go back in recent history and fix your memory. You put the wrong answer under this heading:
Genome complexity: how humans correct errors - dhw, 2020-11-08, 08:41.

Here is the post:
QUOTE: "It is probably most accurate to say that primary and secondary emotions have phenomenal consciousness (experiential feeling), but lack access consciousness (the ability to rationally access, manipulate and reflect upon emotions).

dhw: This is what I mean when I talk of different levels of intelligence/consciousness. But in the context of evolution, the basic drive is not confined to the brain and the exploitation of resources (i.e. finding food) – it also encompasses finding different modes of survival (e.g. avoiding predators, using or building shelters, countering every threat to existence). And I would suggest that this all begins at cellular level, with “phenomenally conscious” cells cooperating over billions of years to form increasingly complex structures, INCLUDING the brain and every other organ we know of and every other life form we know of. This is the “continuum” of evolution that David talks of, as organisms branch out into an ever more variegated bush, with just one of millions of “lines” leading to humans. The cell communities that form the brain itself would have followed precisely the same process of complexification as they responded to new requirements, including control of their new organs. The brains of most life forms would have settled once they had achieved “satisfaction and homeostasis” but, as we know, the human brain continued to expand as “access consciousness” enabled early humans to rationalize and manipulate – not just in terms of reflecting on emotions etc, but also reflecting on and implementing new methods of surviving and/or exploiting their environment.

Please pinpoint what you consider to be “confused”.

Under: "Sensory neurons do more than accept":
QUOTE: "The findings suggest that the sensory cortex is not just sensory, as previously thought. Instead of responding only to stimuli around us, Dr. Maravall's study suggests that the sensory neurons are also involved in processing the meaning of the stimuli, and planning the subsequent behavioural responses."

dhw: Wow, we have cells processing information and planning what to do with it. Sounds like intelligence to me.

DAVID: Why not? God designed them that way.

You could hardly have clearer signs of intelligence than processing information and planning what to do with it. This is the focal point of our discussion and, as an agnostic, I have no problem with your proposal that your God designed the intelligence of cells. ;-)

Genome complexity: how humans correct errors; dhw confusion

by David Turell @, Saturday, November 14, 2020, 21:06 (1231 days ago) @ dhw

DAVID: It is an issue of direct control or second-hand control, and how one views a purposeful God.

dhw: Agreed. How does that make direct control more “logical” than allowing organisms to do their own designing, especially if you claim that your controlling God’s goal was to directly design humans, and he did this by directly designing millions of branches of life that had no connection with humans.

Remember my concept is to design humans over the time evolution took. This is an area of your constant confusion about what I think in regard to God's motives.


dhw: I remain baffled by your reference to “dhw confusion” in the heading of this thread.

DAVID: Go back in recent history and fix your memory. You put the wrong answer under this heading:
Genome complexity: how humans correct errors - dhw, 2020-11-08, 08:41.

Here is the post:
QUOTE: "It is probably most accurate to say that primary and secondary emotions have phenomenal consciousness (experiential feeling), but lack access consciousness (the ability to rationally access, manipulate and reflect upon emotions).

dhw: This is what I mean when I talk of different levels of intelligence/consciousness. But in the context of evolution, the basic drive is not confined to the brain and the exploitation of resources (i.e. finding food) – it also encompasses finding different modes of survival (e.g. avoiding predators, using or building shelters, countering every threat to existence). And I would suggest that this all begins at cellular level, with “phenomenally conscious” cells cooperating over billions of years to form increasingly complex structures, INCLUDING the brain and every other organ we know of and every other life form we know of. This is the “continuum” of evolution that David talks of, as organisms branch out into an ever more variegated bush, with just one of millions of “lines” leading to humans. The cell communities that form the brain itself would have followed precisely the same process of complexification as they responded to new requirements, including control of their new organs. The brains of most life forms would have settled once they had achieved “satisfaction and homeostasis” but, as we know, the human brain continued to expand as “access consciousness” enabled early humans to rationalize and manipulate – not just in terms of reflecting on emotions etc, but also reflecting on and implementing new methods of surviving and/or exploiting their environment.

dhw: Please pinpoint what you consider to be “confused”.

I repeat. What I received from you was comment under the wrong post title answering a different post title comment. I commented on the confusion and straightened out the mix up. Forget the issue, as we proceeded properly after that.


Under: "Sensory neurons do more than accept":
QUOTE: "The findings suggest that the sensory cortex is not just sensory, as previously thought. Instead of responding only to stimuli around us, Dr. Maravall's study suggests that the sensory neurons are also involved in processing the meaning of the stimuli, and planning the subsequent behavioural responses."

dhw: Wow, we have cells processing information and planning what to do with it. Sounds like intelligence to me.

DAVID: Why not? God designed them that way.

dhw: You could hardly have clearer signs of intelligence than processing information and planning what to do with it. This is the focal point of our discussion and, as an agnostic, I have no problem with your proposal that your God designed the intelligence of cells. ;-)

I know you do ;-)

Genome complexity: controlling transposons

by David Turell @, Friday, August 09, 2019, 19:16 (1694 days ago) @ David Turell

Transposons are elements that jump around the genome and may be a driver of evolution, but they most be controlled and not allowed to cause all sorts of disruptions:

https://phys.org/news/2019-08-upcycling-proteins-dna-parasites.html

"...at least half of our genetic material originated from selfish genetic elements such as transposons. Scattered throughout the genomes of plants, fungi and animals, transposons can 'jump' from one genomic position to another. In doing so, they provide an important source of genetic diversity and thereby can promote adaptation of their host. Uncontrolled transposon activity on the other hand leads to widespread DNA damage and mutations, which can result in disease or cell death. To prevent this, organisms have developed effective ways to keep the harmful genome intruders in check.

"The lab of Julius Brennecke at IMBA studies a small RNA-based genome immune system, which suppresses transposon activity in animals. At its core are piRNAs, tiny snippets of genetic information that guide a silencing machinery to find transposons and prevent their jumping. piRNAs are processed from longer RNAs, which must leave the cell nucleus in order to travel to the piRNA production sites in the surrounding cytoplasm. But there is a problem: the nucleus has a quality control system to prevent RNAs that lack molecular maturation signatures from traveling out to the cytoplasm—and piRNA precursors lack all of these molecular signatures.

***

"...the emerging piRNA precursors also utilize heterochromatin to enable the journey from the nucleus to their cytoplasmic destination. A protein called Nxf3, a sister protein of the textbook RNA exporter Nxf1, plays a central role in this process. Nxf3, together with its companion called Bootlegger, smuggles the piRNA precursor from the heterochromatic production sites into the cytoplasm, where it then delivers the RNA cargo to the piRNA production machinery. "The Nxf3 pathway bypasses cellular quality control checkpoints and reveals a novel concept of epigenetically-encoded "itineraries" for sorting genetic information in cells. It is fascinating to see how cells use existing building blocks to construct new pathways, which cope with evolutionary challenges.

***

"Meanwhile, the Brennecke group revealed that Nxf2, another Nxf1 sister protein, is also an essential component of the cellular transposon defense system. Surprisingly, Nfx2 has lost its RNA 'travel guide' function and instead plays a central role in heterochromatin formation at transposon loci. Such heterochromatin formation safe-guards the genome by preventing the transposons from jumping. "It is the first demonstration of an RNA export protein performing an entirely different task compared to its original function," explains Julia Batki,

***

"During evolution, existing structures are frequently duplicated and then converted into something new that could be useful. "Our findings present a remarkable example of 'adaptive radiation' at the protein level. Two copies of the ancestral RNA exporter were repurposed during evolution to fulfil entirely new functions in the cell. Especially when facing an arms race like the one against the fast-evolving genome parasites, it could be very beneficial to quickly innovate new molecular routes that help outrun the genetic competitors," says IMBA group leader Julius Brennecke. "

Comment: Just like feedback loops to control production levels there are complex mechanisms to control activity of DNA segments. Not by chance.

Genome complexity: transposons can change DNA folds

by David Turell @, Friday, January 24, 2020, 21:16 (1526 days ago) @ David Turell

More junk DNA turns out to have useful activity:

https://phys.org/news/2020-01-genes-stabilize-dna-patterns.html

"'Jumping genes"—bits of DNA that can move from one spot in the genome to another—are well-known for increasing genetic diversity over the long course of evolution. Now, new research at Washington University School of Medicine in St. Louis indicates that such genes, also called transposable elements, play another, more surprising role: stabilizing the 3-D folding patterns of the DNA molecule inside the cell's nucleus.

***

"Studying DNA folding in mouse and human blood cells, the researchers found that in many regions where the folding patterns of DNA are conserved through evolution, the genetic sequence of the DNA letters establishing these folds is not. It is ever so slightly displaced. But this changing sequence, a genetic turnover, doesn't cause problems. Because the structure largely stays the same, the function presumably does, too, so nothing of importance changes.

"'We were surprised to find that some young transposable elements serve to maintain old structures," said first author Mayank N.K. Choudhary, a doctoral student in Wang's lab. "The specific sequence may be different, but the function stays the same. And we see that this has happened multiple times over the past 80 million years, when the common ancestors of mice and humans first diverged from one another."

"The fact that a new transposable element can insert itself and serve the same role as an existing anchor creates a redundancy in the regulatory portions of the genome—regions of the DNA molecule that determine how and when genes are turned on or off.

"According to the researchers, this redundancy makes the genome more resilient. In providing both novelty and stability, jumping genes may help the mammalian genome strike a vital balance—allowing animals the flexibility to adapt to a changing climate, for example, while preserving biological functions required for life, protecting against the DNA damage that is wrought by living and reproducing on Earth over the span of deep time, measured in tens to hundreds of millions of years.

"Even so, the researchers were careful to distinguish between portions of the genome that hold genes responsible for producing proteins and the rest of the genome. In genes that code for proteins, the genetic sequence and the structure are both conserved, and this study does not contradict that. However, the new research suggests that jumping genes in the non-protein coding areas of the genome follow different rules of conservation than the protein-coding genes.

"'Our study changes how we interpret genetic variation in the noncoding regions of the DNA," Wang said. "For example, large surveys of genomes from many people have identified a lot of variations in noncoding regions that don't seem to have any effect on gene regulation, which has been puzzling. But it makes more sense in light of our new understanding of transposable elements—while the local sequence can change, but the function stays the same.

"'We may need to revisit these types of studies in light of the new understanding we now have of transposable elements," he added. "We have uncovered another layer of complexity in the genome sequence that was not known before.'"

comment: it seems as if the researchers were surprised at this newly found genome complexity. I am not, and am sure the knowledge of more complexity will just grow and grow, further indicating the need for design and a designer.

Genome complexity: a new DNA repair mechanism found

by David Turell @, Sunday, April 07, 2019, 05:07 (1818 days ago) @ Balance_Maintained

Another way of repairing DNA is found:

https://phys.org/news/2019-04-unjamming-genome-dna-gene-regulatory.html

"RNA polymerase II (RNAPII)—the enzyme that produces RNA from a DNA template—can become stuck due to damage to the DNA template, and these jams must be cleared to restore gene expression and normal cell function. New research shows that the master regulatory complex, "Ccr4-Not," performs this task, associating with RNAPII during the transcription of RNA from DNA and marking RNAPII for degradation when it becomes stuck, allowing the DNA to be repaired and normal cell function to resume.

***

"'The Ccr4-Not complex is involved in nearly every step of this process from start to finish. Our new research shows that this complex has an additional function that helps maintain normal cellular function when something goes wrong during transcription."

"During the transcription of RNA from DNA, RNAPII—itself a large complex made up of multiple protein subunits—travels along the strand of DNA reading the ATCG sequence and producing a complementary strand of RNA. If the RNAPII encounters DNA damage, which can be caused by UV radiation and other sources, it can become stuck and prevent trailing polymerases from completing transcription of the gene, similar to how a stalled car prevents traffic behind it from flowing. If this jam cannot be cleared, multiple RNAPIIs transcribing the same gene can start to pile up in a sort of traffic jam preventing the DNA from being repaired and hampering cell function.

"'The clearing of stuck RNAPII is an essential process for normal cell function," said Reese.
"'Defects in this pathway have been associated with a number of diseases and human syndromes, such as Cockayne syndrome—a neurodegenerative disorder that results in growth failure, neurological developmental defects, and sensitivity to UV light.

***

"'Previous studies had implicated Ccr4-Not in helping cells cope with DNA damage," said Reese. "Mutating members of the Ccr4-Not complex makes cells more sensitive to agents that damage the genome, but because Ccr4-Not is involved in so many aspects of gene regulation it wasn't clear until now what its precise role was. The fact that Ccr4-Not recruited the destruction machinery to RNAPII was a surprisi'ng result, and suggests it acts as a tow truck to remove traffic jams throughout the genome. "

Comment: Same point as before. Once DNA is in control the repair mechanism must also be in control or life does not survive. Development of all parts at once implies only design can accomplish this.

Genome complexity: retroviruses are a real part of us

by David Turell @, Monday, April 13, 2020, 01:21 (1447 days ago) @ David Turell

And play major roles in evolution:

https://inference-review.com/article/the-yin-and-yang-of-the-genome#endnote-7

"Humans are, all of us, part retrovirus. Roughly 8% of the DNA in human cells is retroviral in origin: the relics of ancient infections in the germ line of our ancestors. This compares to the figure of 1.5% of the genome that encodes all the proteins that function to keep us alive. It is sobering to think that the double helix is really their world, these little parasites. We are just living in it.

***

"Viruses composed of RNA and relying on reverse transcriptase and a proviral DNA sequence intermediately became known as retroviruses....Three major enzymes comprise the pol: reverse transcriptase (RT), retroviral integrase (IN), and retroviral protease (PR). RT, of course, copies RNA to DNA. IN integrates the resulting DNA provirus into the host. PR is a protein that cuts long viral amino acid chains at precise locations.

***

"By the 1980s, the basic life cycle of the retrovirus was finally understood. A retrovirus attaches to a host cell by way of spikes on its surface: membranes fuse, the viral core is dumped into the cell, and reverse transcription occurs. The DNA provirus is then integrated, proviral promoter sequences hijack cellular transcription proteins, and mRNAs are produced and processed. Most mRNAs are translated into long amino acid chains; the requisite components self-assemble and bud off from the cell. After budding, PR cuts some of the long amino acid chains at the right spots; the freshly cut proteins condense, and the lifecycle is completed.

***

"Viruses are nefarious and well-made. No invasion is haphazard. A retrovirus has just the right sequence of molecular keys fitting just the right sequence of cellular locks at just the right times. Half of a virus, or half of its proteins, would never make it. Where did viruses and retroviruses come from?

"Skalka notes that “no clear explanation for the origin of all viruses exists.”

***

"Skalka turns her attention to the dual nature of the retrovirus. The virus as poison needs no defense: it is obvious. But how could a retrovirus ever be a gift useful to an organism? In several ways, actually. The first is evolutionary. Retroviruses and ERVs increase the pool of available genetic variation. The richer the variation, the better the evolvability.

***

"If it were not for retroviruses, humanity might still be primitive hunter-gatherers without civilization; our immune systems would be weaker; we would be hatching from eggs. How so? A regulatory segment in an ERV controls a copy of the enzyme amylase, which allowed humans to incorporate starch into their diets. Control of amylase opened the potential for the species to become farmers instead of hunter-gatherers. Similarly, HERVs in the major histocompatibility complex have shaped the evolution of the immune system. And certain ERV genes were recruited during the evolution of the mammalian placenta: specifically those assisting with cell fusion and immune suppression, which is co-opted for the protection of the fetus. (my bold)

***

"Viruses want a sure thing, and so tend to target stable host genes unlikely to change; in response, the host is forced to change them, but in noncritical regions that may help repel the virus while doing minimal damage. In humans, roughly 5% of codon changes in mundane housekeeping genes are due to the arms race with viruses. In other mammals, it is an astounding 30%. (my bold)

***

"By using retroviruses as vectors in conjunction with the remarkable CRISPR-Cas system, which is a defense system against viruses in some prokaryotic organisms, virtually any DNA segment in any cell type can be targeted and replaced. This has massive potential for treating genetic diseases. However, it also involves ethical issues, as the system could be used to sculpt the genetic architecture of human embryos and make them into designer children. This again returns to the recurring theme of the book: the dual nature of retroviruses. Viruses deform and kill millions, but also provide opportunities to help millions. The principle is illustrated with no greater irony than in the case of HIV. Humans are now using genetically modified HIV particles as vectors to treat HIV symptoms, as well as other genetic diseases."

Comment: Note my bolds. The first shows that retroviruses are part of God's armamentarium in managing evolution. And note that allows us to manage problems. Is that a purposeful gift from God? The second shows another major difference in humans from other primates, creating more of our specialness. This is taken from a book review.

Genome complexity: getting X and Y together

by David Turell @, Saturday, May 30, 2020, 00:12 (1400 days ago) @ David Turell

Y is tiny but active in the control of this process:

https://www.sciencedaily.com/releases/2020/05/200528160557.htm

"As chromosomes go, X and Y make an unlikely pair. The X is large and contains thousands of genes critical for life. The Y, by contrast, is little more than a nub. Its main purpose is to provide the instructions for initiating male development and making sperm. Yet these two very different chromosomes must work together if they are to meet and pair up properly during meiosis -- the special form of cell division that creates sperm and egg.

***

"Breaking is a theme of meiosis. During this process, every chromosome we got from our mothers lines up with every chromosome we got from our fathers and the two swap segments. Before this swapping can occur, the DNA in the chromosomes must be deliberately broken. The regions that are swapped are "homologous" -- they're found in the same place along the chromosome and contain the same genes (although the particular DNA sequence of each gene may be slightly different).

"Homologous recombination is vastly more challenging for males because most of the X chromosome has nothing to pair with. In fact, only a very tiny portion of the already tiny Y chromosome has any homology with the X. This region is called the pseudoautosomal region (PAR), and it's critical for making sure that X and Y find their way into different sperm cells.

"Scientists have known for a long time that the PAR undergoes breaking and swapping of segments at a level that far outpaces what one would expect, given its size.

"'On most chromosomes, DNA double-strand breaks typically occur once every 10 million base pairs," says Scott Keeney, a molecular biologist at SKI, who studies this phenomenon. "The PAR in mice is less than 1/10 that size but it still manages to undergo frequent double-strand breaks."

***

"The key to proper pairing of X and Y, they discovered, is a repeated sequence of DNA in the PAR that attracts several double-strand break-related proteins to this region. These protein clusters -- which Dr. Acquaviva dubbed "blobs" -- change the architecture of the chromosome in this region in such a way that the PAR becomes, as the authors put it, "the hottest area of double-strand break formation in the male mouse genome."

***

"'At first glance, the blobs just look like a mess you might see in the microscope if the experiment didn't work," Dr. Acquaviva says. "But they turned out to be completely predictable in number, timing, and location, so it became clear that in reality they are very complex structures that the cell builds on purpose." (my bold)

"In fact, he says, these blobs were key to understanding how the PAR DNA is tethered as short loops to the linear axis that is the structural backbone of the chromosome.

"Though the X chromosome also has this same repeated DNA sequence, the two X chromosomes in female meiosis typically do not recombine at this region. Why not? The SKI scientists show that it is because pairing between other regions of the X tends to happen first and directly opposes breakage at the PAR."

Comment: The X and Y chromosome are involved separately in purposeful activity (note the bold) but each does its own thing before the changes each created for itself produces the desired result. Not by chance. Must be designed. And as a result looks like intelligent activity. I can't imagine sex cells cooking this up on their own. The use of sexual reproduction evolved and produced a greater variety of diversity, but it obviously created such problems, only a designer could have produced it.

Genome complexity: slicing and dicing DNA for germ cells

by David Turell @, Friday, August 13, 2021, 19:18 (959 days ago) @ David Turell

Sperm and egg must have DNA mixed up to to pass on proper mixed Mother and Dad inheritance:

https://phys.org/news/2021-08-brca2-protein-complex-important-dna.html

***

"The initials BRCA2 may be best known for a gene associated with many cases of breast cancer, and the protein encoded by the BRCA2 gene is critical to repairing breaks in DNA.

"The breakdown of this interaction is a hallmark of many cancers. Now, U-M scientists have determined the structure of a complex of two proteins—BRCA2 together with MEILB2—that allows repairs to happen efficiently in cells undergoing cell-splitting, called meiosis. Their results, reported in Nature Structural and Molecular Biology, have major implications for cancer and infertility.

***

"In germ cells—the cells that give rise to sperm or eggs—DNA breaks occur in every chromosome before the cells undergo meiosis. The breaks ensure mixing of genes to create genetic diversity rather than exact copies of the parents. In meiosis, each germ cell splits twice so that each egg or sperm ends up with only one copy of each chromosome. Then when egg meets sperm, the embryo has the right number of chromosome pairs.

"Before the first split occurs, the chromosomes in the germ cell pair up tightly and then each chromosome within a pair breaks and rejoins with pieces from its partner to exchange genes in a process called crossover. Then all these DNA breaks need to be rejoined quickly.

Think of a sandwich, Nandakumar explains. The "bun" is composed of four identical copies of a protein called MEILB2 on the top and bottom, with the two BRCA2 proteins between. The MEILB2 protein sandwich carries the BRCA2 protein precisely to the DNA break points.

***

"'While we have known BRCA2 was necessary for DNA recombination in meiosis, we didn't know how it was able to do this critical job efficiently," Nandakumar said. "The MEILB2 that is part of this repair complex is only supposed to be present in cells that undergo meiosis but MEILB2 has also been found in several cancers. It may be that MEILB2 is very efficiently 'hijacking' the BRCA2 in cancer cells, preventing proper repair of the DNA."

"Without other factors usually found in meiotic cells, the BRCA2 in these MEILB2-positive cancers might not get to the DNA breakpoints."

Comment: another highly complex process in making egg and sperm that runs at extremely fast micro-second rates. Must be designed all at once not by any stepwise process. Shows how there must be a designer.

Genome complexity: controlling plant growth

by David Turell @, Thursday, April 28, 2022, 22:10 (701 days ago) @ David Turell

A special enzyme is involved:

https://phys.org/news/2022-04-enzyme-strigolactone-hormone-growth.html

"As sessile organisms, plants have to continually adapt their growth and architecture to the ever-changing environment. To do so, plants have evolved distinct molecular mechanisms to sense and respond to the environment and integrate the signals from outside with endogenous developmental programs.

***


"The work stems from a study by Shabek, published in Nature in 2018, unraveling molecular and structural changes in an enzyme, MAX2 (or D3) ubiquitin ligase. MAX2 was found in locked or unlocked forms that can recruit a strigolactone sensor, D14, and target for destruction a DNA transcriptional repressor complex, D53. Ubiquitins are small proteins, found in all eukaryotes, that "tag" other proteins for destruction within a cell.

***

"They found that in the unlocked conformation, MAX2 can target the repressor proteins and biochemically decorate them with small ubiquitin proteins, tagging them for destruction. Removing these repressors allows other genes to be expressed—activating a massive gene network that governs shoot branching, root architecture, leaf senescence, and symbiosis with fungi, Shabek said.

"Sending these repressors to the proteasome disposal complexes requires the enzyme to relock again. The team also showed that MAX2 not only targets the repressor proteins, but once it is locked, the strigolactone sensor itself is destroyed, returning the system to its original state.

"Finally, the study uncovered the key to the lock, an organic acid metabolite that can directly trigger the conformational switch."

Comment: Once again, a complex mechanism which involves a giant enzyme molecule o drive the process. Without these specialized molecules, there would be no life. Design is required.

Genome complexity: retroviruses in embryology

by David Turell @, Tuesday, January 30, 2024, 15:37 (59 days ago) @ David Turell

They control pluripotency:

https://www.sciencealert.com/embryo-development-linked-to-a-500-million-year-old-viral-...

"A critical early stage of embryonic development has been linked to a virus that mixed with the ancestral DNA of complex organisms like ourselves more than 500 million years ago.

"Genetic material from endogenous retroviruses – which infected the earliest organisms on Earth, leaving markers in our DNA – is estimated to make up around 8 to 10 percent of the modern human genome.

"'Until recently, these viral remnants were considered to be junk DNA, genetic material that was unusable or even harmful," says biologist Sergio de la Rosa, from CNIO. (my bold)

***

"Through a detailed study of mouse models, the team was able to identify a retroviral protein called MERVL-gag, which helps manage the pace of embryo development just a few hours after fertilization.

"The key development in question is when the first few totipotent cells (capable of becoming any of the cells that form the entire organism) give rise to pluripotent cells (capable of becoming cells that form any tissues of the body, but not placental tissue).

"This gradual process of specialization in the embryo is what turns a blob of cells into either a cat, a sea cucumber, an earthworm, or a human being, and the researchers showed how MERVL-gag influences a gene called URI – thought to be essential in enabling molecules to become pluripotent.

"'It is a totally new role for endogenous retroviruses," says Djouder. "We discovered a new mechanism that explains how an endogenous retrovirus directly controls pluripotency factors."

"The team found high levels of expression of the MERVL-gag protein in the early totipotency phase of embryo growth, with these levels then steadily decreasing as URI becomes more influential on the behavior of cells.

"What we're seeing here is a careful balance between proteins, genes, and pluripotency, the result of hundreds of millions of years of evolution, and none of it would be possible without an ancient virus.

***

"'We are starting to realize that these retroviruses, which have co-evolved with us over millions of years, have important functions, such as regulating other genes," says de la Rosa. "It's an extremely active field of research.'"

Comment: Well, more 'junk DNA' is not. It fits my thesis everything happens for a reason. It also fits my thesis we have viruses because they help code DNA, with good and bad results.

Genome complexity in embryology:organizer

by David Turell @, Saturday, June 04, 2016, 21:05 (2855 days ago) @ David Turell

As the embryo forms it must have a guide to its axes, front, back, up, down, head and tail. That organizer is over 600 million years old, appearing before bilatarians, and well before the pre-Cambrians. It is part of the support for the structuralism, patterns theory of evolution:-https://www.sciencedaily.com/releases/2016/06/160601110739.htm-"Cells need to 'know' where they are in relation to all other cells in order to give rise into the correct cell types and tissues. The so-called 'organizer' is responsible for the formation of these body axes. Developmental biologists have shown that the molecular principles of the organizer are much more ancient than previously thought. The same signals were used already in the common ancestor of sea anemones and vertebrates 600 million years ago. -"In humans and in animals, the correct position of tissues, organs and appendages is essential. Two body axes (the head-tail and the back-belly axes) usually define this position by generating a coordinate system, which supplies each cell in the body with its precise address. Thus, for example, the vertebrate central nervous system is always located on the back, and the intestinal tract on the belly of the animal.-"In vertebrate early development, an "organizer" forms in the region of the primitive mouth (the blastopore) of the embryo. This organizer is responsible for guiding axis formation of the organism. Its discovery won Hans Spemann a Nobel Prize in 1935. The organizer tissue instructs the surrounding cells to take part in body axes development, enforcing a certain developmental fate on them. Without an organizer, the embryo would not know where the head, the tail, the back and the belly should be. Mistakes in the regulation of body axes can lead to severe developmental defects, for example to the formation of Siamese twins.-"In the last 25 years, the researchers largely elucidated the genetic underpinnings of this very particular part of the vertebrate embryo. The widespread assumption was that the organizer was a specific vertebrate feature, since it was not readily observable in insect or worm embryos.-"The team of Grigory Genikhovich and Ulrich Technau from the Department of Molecular Evolution and Development of the University of Vienna now demonstrated that not only the principle of the organizer but also its molecular underpinnings are much older than previously supposed. "By performing transplantation experiments and molecular analyses we have found a blastoporal organizer in the embryos of the sea anemone Nematostella vectensis. For inducing axes, it uses the same class of signaling molecules as the vertebrate organizer," explains Technau. "We conclude that this principle of the regulation of the embryonic axes existed already in the common ancestor of vertebrates and sea anemones more than 600 million years ago.'"-Comment: This fits my concept of pre-planning which in current terms is structuralism and patterns theory

Genome complexity in embryology: new theory

by David Turell @, Friday, June 10, 2016, 02:28 (2850 days ago) @ David Turell

Why not use a study of embryology to try to explain how evolution develops complexity:-An abstract:-Abstract: Today there is a very wide consensus on the idea that embryonic development is the result of a genetic programme and of epigenetic processes. Many models have been proposed in this theoretical framework to account for the various aspects of development, and virtually all of them have one thing in common: they do not acknowledge the presence of organic codes (codes between organic molecules) in ontogenesis. Here it is argued instead that embryonic development is a convergent increase in complexity that necessarily requires organic codes and organic memories, and a few examples of such codes are described. This is the code theory of development, a theory that was originally inspired by an algorithm that is capable of reconstructing structures from incomplete information, an algorithm that here is briefly summarized because it makes it intuitively appealing how a convergent increase in complexity can be achieved. The main thesis of the new theory is that the presence of organic codes in ontogenesis is not only a theoretical necessity but, first and foremost, an idea that can be tested and that has already been found to be in agreement with the evidence. -Comment: I can't get the rest without $$$, but it is a great idea to find the underlying mechanism.

Genome complexity in embryology: mitochondria

by David Turell @, Monday, June 27, 2016, 14:30 (2832 days ago) @ David Turell

Only the mother's mitochondria end up in the offspring. The mechanism is found in C. elegans and it is assumed this may be the way it worksat all lev els of development:-http://www.the-scientist.com/?articles.view/articleNo/46414/title/Why-Paternal-Mitochondria-Aren-t-Passed-on-to-Offspring/&utm_campaign=NEWSLETTER_TS_The-Scientist-Daily_2016&utm_source=hs_email&utm_medium=email&utm_content=31024464&_hsenc=p2ANqtz--mMLVl8aHluBiiWWHuQrebGC2LoNlWNFNAAzuxS8omZG6yXxY95p9Z9XEnvP21r9dS6OSBl7Lv997QRUSOMSJx2kv8Jg&_hsmi=31024464/-"Researchers have uncovered a clue as to why a mother's mitochondria are passed on to her offspring while the father's are not. Studying sperm cells from the roundworm Caenorhabditis elegans, researchers at the University of Colorado, Boulder, and colleagues found that a gene called cps-6 encodes a mitochondrial endonuclease that degrades paternal mitochondrial DNA (mtDNA) following fertilization of an egg. Delaying this process can be fatal to the embryo, the team reported yesterday (June 23) in Science.-***-"Qinghua Zhou of the University of Colorado and colleagues examined the C. elegans cells using electron microscopy and tomography, finding that the paternal mitochondria started to self-destruct even before they were engulfed by autophagosomes. Using RNA analysis, the researchers identified cps-6 as an important part of this process. When this gene was removed, the paternal mitochondria persisted, resulting in increased embryo mortality.-“'This provides evidence that persistence of paternal mitochondria compromises animal development and may be the impetus for maternal inheritance of mitochondria,” the researchers wrote in their paper.-"It remains to be seen whether the same process occurs in humans, biologist Vincent Galy of the Pierre and Marie Curie University in Paris, who did not take part in the study, told Science News. “You could imagine there's a similar mechanism, but there's no demonstration yet,” he said."-Comment: Why are Daddy's toxic? Not known.

Genome complexity in embryology: nerve routes

by David Turell @, Monday, April 24, 2017, 15:09 (2531 days ago) @ David Turell

Guiding axons to the proper spots requires chemical guidance:

https://www.sciencedaily.com/releases/2017/04/170420162153.htm

"As an embryo grows, neurons -- the cells in the nervous system -- extend axons into the developing spinal cord. Axons are then guided to reach other areas of the body, such as the brain, to establish a functioning nervous system. It has been generally understood that various guidance cues, which are cellular molecules such as proteins, either attract or repel axon growth as the axons reach out from neurons to find their destination in the nervous system.

"Previous research suggested that a particular guidance cue, called netrin1, functions over a long distance to attract and organize axon growth, similar to how a lighthouse sends out a signal to orient a ship from afar. However, previous research also shows that netrin1 is produced in many places in the embryonic spinal cord, raising questions about whether it really acts over a long distance. Most notably, netrin1 is produced by tissue-specific stem cells, called neural progenitors, which can create any cell type in the nervous system.

***

"They found that neural progenitors organize axon growth by producing a pathway of netrin1 that directs axons only in their local environment and not over long distances. This pathway of netrin1 acts as a sticky surface that encourages axon growth in the directions that form a normal, functioning nervous system."

Comment: neurons in the lumbar spine must reach the feet of the newborn, perhaps eight to ten inches of travel accurately reaching the proper spots. The same is true for blood vessels. We have no idea how the genome directs all of this, but the chemical guides are becoming discovered as this study shows.

Genome complexity in embryology: nerve routes

by Balance_Maintained @, U.S.A., Tuesday, April 25, 2017, 00:43 (2531 days ago) @ David Turell

Psalms 139:14 I praise you because I am fearfully and wonderfully made; your works are wonderful, I know that full well.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity in embryology: nerve routes

by David Turell @, Tuesday, April 25, 2017, 01:01 (2531 days ago) @ Balance_Maintained

Tony: Psalms 139:14 I praise you because I am fearfully and wonderfully made; your works are wonderful, I know that full well.

God designed it all. I don't see how it could work any other way, given the complexity especially in developmental embryology, as well as the final result.

Genome complexity in embryology: egg starting

by David Turell @, Tuesday, July 11, 2017, 23:41 (2453 days ago) @ David Turell

mRNA's from the mother helps get the fertilized egg started:

https://phys.org/news/2017-06-elegant-transition-egg-embryo.html

"The transition from an egg to a developing embryo is one of life's most remarkable transformations. Yet little is known about it. Now Whitehead Institute researchers have deciphered how one aspect—control of the all-important translation of messenger RNAs (mRNAs) into proteins—switches as the egg becomes an embryo. That shift is controlled by a beautiful mechanism, which is triggered at a precise moment in development and automatically shuts itself off after a narrow window of 20 to 90 minutes.

"As an egg develops, it stockpiles mRNAs from the mother because it will not have time to create new mRNAs during the rapid development of a very early embryo. When fertilized the egg becomes an embryo, the stashed maternal mRNAs are pressed into service for a brief window before the embryo starts transcribing its own mRNAs. This change occurs very early; in humans, only two to four cell divisions occur before this transition is executed.

" In the current research, Orr-Weaver and her lab determined that key to the transition are the three molecules that form the enzyme PNG kinase: PNG, PLU, and GNU. Orr-Weaver describes PNG and PLU as "tight buddies" that are always locked together, including in the mature egg. At that point in development, GNU has phosphate molecules tacked to it, which impede its binding to PNG-PLU.

"When an egg is activated, levels of another enzyme that adds phosphates to GNU in the egg precipitously drop, allowing GNU to lose its phosphates and bind to PNG-PLU. Once together, the trio comprises the PNG kinase that triggers the translational control of the maternal mRNAs. Because PNG kinase also triggers the break down of GNU, the kinase self-destructs, which quickly and irreversibly squelches the translation of maternal mRNAs. This elegant feedback loop and the switch it controls are described in an article in eLife. (my bold)

***

"Although she now has as greater understanding of how translation is turned on and off during very early embryonic development, Orr-Weaver is intrigued by how the switch is linked to the translation machinery.

"'PNG is a kinase, which means it controls things by what it phosphorylates," says Orr-Weaver, who is also an American Cancer Society Research Professor of biology at MIT. "So the big question is what proteins does it phosphorylate? Finding that out is the next big phase of this project.'"

Comment: Note my bold. A feedback loop must develop all at once with all of it. The enzyme is a giant molecule. Evolution did not hunt and peck for it. It has a specific purpose fro which it is designed. That is the key point. A system like this requires a designer!

Genome complexity in embryology: egg starting

by Balance_Maintained @, U.S.A., Thursday, July 13, 2017, 05:53 (2451 days ago) @ David Turell

David
...
"When an egg is activated, levels of another enzyme that adds phosphates to GNU in the egg precipitously drop, allowing GNU to lose its phosphates and bind to PNG-PLU. Once together, the trio comprises the PNG kinase that triggers the translational control of the maternal mRNAs. Because PNG kinase also triggers the break down of GNU, the kinase self-destructs, which quickly and irreversibly squelches the translation of maternal mRNAs. This elegant feedback loop and the switch it controls are described in an article in eLife. (my bold)

***

"Although she now has as greater understanding of how translation is turned on and off during very early embryonic development, Orr-Weaver is intrigued by how the switch is linked to the translation machinery.

"'PNG is a kinase, which means it controls things by what it phosphorylates," says Orr-Weaver, who is also an American Cancer Society Research Professor of biology at MIT. "So the big question is what proteins does it phosphorylate? Finding that out is the next big phase of this project.'"

Comment: Note my bold. A feedback loop must develop all at once with all of it. The enzyme is a giant molecule. Evolution did not hunt and peck for it. It has a specific purpose fro which it is designed. That is the key point. A system like this requires a designer!

You know, it is getting to the point where I don't even feel the need to argue for God here because you are doing such a beautiful job of it for me. :-D

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

Genome complexity in embryology: egg starting

by David Turell @, Thursday, July 13, 2017, 15:23 (2451 days ago) @ Balance_Maintained


David: Comment: Note my bold. A feedback loop must develop all at once with all of it. The enzyme is a giant molecule. Evolution did not hunt and peck for it. It has a specific purpose fro which it is designed. That is the key point. A system like this requires a designer!


Tony: You know, it is getting to the point where I don't even feel the need to argue for God here because you are doing such a beautiful job of it for me. :-D

Thank you.

Genome complexity in embryology: stem cell action

by David Turell @, Friday, July 28, 2017, 19:20 (2436 days ago) @ David Turell

This careful and complex study follows stem cells as they differentiate. They make decisions along the way:

http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2001867

Abstract

"Individual cells take lineage commitment decisions in a way that is not necessarily uniform. We address this issue by characterising transcriptional changes in cord blood-derived CD34+ cells at the single-cell level and integrating data with cell division history and morphological changes determined by time-lapse microscopy. We show that major transcriptional changes leading to a multilineage-primed gene expression state occur very rapidly during the first cell cycle. One of the 2 stable lineage-primed patterns emerges gradually in each cell with variable timing. Some cells reach a stable morphology and molecular phenotype by the end of the first cell cycle and transmit it clonally. Others fluctuate between the 2 phenotypes over several cell cycles. Our analysis highlights the dynamic nature and variable timing of cell fate commitment in hematopoietic cells, links the gene expression pattern to cell morphology, and identifies a new category of cells with fluctuating phenotypic characteristics, demonstrating the complexity of the fate decision process (which is different from a simple binary switch between 2 options, as it is usually envisioned)."

Author summary

"Hematopoietic stem cells are classically defined as a specific category of cells at the top of the hierarchy that can differentiate all blood cell types following step-by-step the instructions of a deterministic program. We have analysed this process, and our findings support a much more dynamic view than previously described. We apply time-lapse microscopy coupled to single-cell molecular analyses in human hematopoietic stem cells and find that fate decision is not a unique, programmed event but a process of spontaneous variation and selective stabilisation reminiscent of trial–error processes. We show that each cell explores (at its own pace and independently of cell division) many different possibilities before reaching a stable combination of genes to be expressed. Our results suggest, therefore, that multipotency seems to be more like a transitory state than a feature of a specific cell category."

A simpler take:

https://cosmosmagazine.com/biology/becoming-a-cell

"At every moment from fertilisation onwards the creation of a human body requires cells, generated by cell division, to “choose” which of the many possible kinds of cell they will become. How do they decide?

"One common view is that there was some step-by-step decision-making process or algorithm to follow. New research from a team of French biologists led by Alice Moussy of the Ecole Pratique des Hautes Etudes suggests that this is not the case.

"The researchers microscopic video recordings and single-cell molecular analyses to observe the process of hematopoietic stem cells (cells which can become any one of a number of different kinds of blood cell). They discovered that rather than a single decision event, cell specialisation was a dynamic process involving spontaneous fluctuations between alternative cell states and selective stabilisation of certain states.

"In a sense it is a trial-and-error process: each cell independently “tries out” different molecular possibilities – via turning on and off different genes – before settling into a stable state of activated genes and a corresponding shape."

Comment: Stem cells seem in this study to have trouble making up their 'minds', but it all works out in the end with 9usually) all the cells in all the right places. The cells are influenced also by mechanical forces from other cells as well as hormonal and chemical signals. As the result they are buffeted in may ways as the embryo develops. All of these ways are still being actively studied since making a fully developed individual is not fully understood. The underlying process is one automatic system: all newborns look generally alike.

Genome complexity in embryology: non-DNA information

by David Turell @, Sunday, June 03, 2018, 20:41 (2126 days ago) @ David Turell

Carried by positional information, membrane information and electric field information:

https://evolutionnews.org/2018/06/life-exponential-life-exhibits-intelligent-design-at-...

" After the nucleus duplicates, the fertilized egg divides into two daughter cells. If the plane of division corresponds to A, each daughter cell inherits not only a nucleus but also portions of all four regions of cortical information. .. But if the plane of division corresponds to B or C, the daughter cells do not inherit a full set of cortical information, and their development is blocked even if they each contain all the necessary DNA.


"Regional differences in cells and embryos can be specified in other ways besides localization of RNAs in the cortex. Two of those ways have been studied in great detail: the “sugar code” and the “bioelectric code.”

"Most proteins in living cells — including those in membranes — are chemically bonded to carbohydrates called “glycans”. The nucleotides in DNA are linked together end-to-end in a linear molecule, so DNA sequence information is one-dimensional. In living cells, the subunits in proteins (with a few exceptions) are also linked in a linear chain. But glycans can be linked together in complex three-dimensional ways, so their information-carrying capacity exceeds that of DNA and proteins by many orders of magnitude.

"The information carried by glycans has been called the “sugar code.” The sugar code is “interpreted” by proteins called lectins, which “recognize” specific three-dimensional structures of glycan molecules. Glycans and lectins play an essential role in communication among cells and help to guide cell movements in a developing embryo. Experiments have shown that membrane patterns of glycans change in the course of embryo development.

"In addition to the sugar code, probably all living cells generate electric fields across their membranes. They do this by pumping charged ions through channels in their membranes, creating a “bioelectric field.” The pattern of membrane channels determines the form of the bioelectric field, and the form of the field changes during embryo development.

"Bioelectric fields are correlated with important developmental events. In frog embryos, for example, large ionic currents start flowing out of the sites where the hind limbs will develop long before the limbs appear.

"Many experiments conducted since the 1980s have confirmed that disrupting bioelectric fields causes disruptions in development. .. The spots where eyes normally form are more highly charged than the surrounding tissue; if the charge is neutralized, the eyes that develop are small or deformed. Sometimes, eyes develop elsewhere on the tadpole’s body, including its tail.

"How do electric fields influence development? In the 1980s, biologists exposed embryonic cells to artificial electric fields of the same strength as ones the cells generate naturally. Some types of cells migrated toward the positive pole, while other types migrated to the negative pole, suggesting that one way bioelectric fields affect embryo development is by directing cell movements.

"In 1995, biologists Riyi Shi and Richards Borgens concluded that bioelectric fields “may provide a three dimensional coordinate system” that helps to specify form in embryos. In 2013, biologists AiSun Tseng and Michael Levin wrote that such fields may provide “templates of shape,” and that a full understanding of embryo development will probably require cracking the “bioelectric code.”

"So localized RNAs in the cortex, glycan patterns on the membrane, and bioelectric fields generated by ion channels in the membrane all carry spatial information. Although individual molecules may be specified by DNA, their three-dimensional patterns are not. Taken together, these patterns constitute a “membrane code” that is independent of DNA sequences.

"In 1983, biologist Robert Poyton suggested that biological membranes carry “spatial memory,” the units of which are spatially localized proteins. Poyton wrote: “Realizing that genetic memory is one-dimensional, along a DNA molecule, whereas spatial memory is likely to be two-dimensional, along membrane surfaces, and three-dimensional within the cellular interior, it is probable that spatial memory is more complicated and diverse than genetic memory.”

"In 2004, biologist Thomas Cavalier-Smith wrote that the idea that DNA contains all the information needed to make an organism “is simply false.” Animal development creates a complex three-dimensional multicellular organism not by starting from the linear information in DNA… but always starting from an already highly complex three-dimensional unicellular organism, the fertilized egg.”

"So the membrane code carries essential biological information that is independent of DNA.

***

"But the existence of the membrane code shows that the Central Dogma is false. And the materialistic idea that evolution is unguided cannot account for the complex specified information in DNA, much less for the extensive complex specified information in the membrane code. Just as the information in DNA points to design, so does the information beyond DNA. "

Comment: Embryology is too complex for chance. It involves using spatial, mechanical molecular shale and electrical field information. After life evolved it had to use embryos when sex appeared. Embryology is as much a miracle as the start of life itself.

Plant embryology: leaf making feedback controls

by David Turell @, Wednesday, June 06, 2018, 19:42 (2123 days ago) @ David Turell

All life regulates itself by circular feedback loops, especially in creating new parts:

https://www.sciencedaily.com/releases/2018/06/180606132652.htm

"During growth, plants constantly form new leaves, branches, and roots over weeks, months, and years. These are initially formed via cell division, where cells develop in highly complex, yet orderly processes. One result of these developmental programs is the vascular tissue of the plants, which is visible to the human eye in the form of leaf veins. Vascular tissue pervades the entire plant body, supplying the plant with water and salts from the ground via the xylem, and with metabolic products such as sugars from photosynthesis via the phloem.

***

"'Back in 2009, the team in Lausanne demonstrated that plants which were lacking a certain protein (BRX) have problems forming phloem cells," states co-author Lanassa Bassukas .."At the same time, they also observed that it has a highly sensitive response to the plant hormone auxin. Depending on whether the auxin value was low or high, the protein was located in the cell membrane or was degraded inside the cell."

"This became relevant when the TUM researchers discovered a new regulator called PAX. With the help of this regulator, the hormone auxin can be transferred out of the cell via transporter proteins. Just as in plants with a defect in the BRX protein, plants without PAX had fewer phloem cells.

"'For us, it was noteworthy, on the one hand, that the PAX regulator could be retarded by the BRX protein, and on the other, that PAX became more active as the auxin level in the cell increased," explains Martina Kolb and Ulrich Hammes from TU Munich, who provided important findings for the new model with their auxin transporter studies.

"According to their findings, auxin initially accumulates in a newly developed cell. This is because BRX prevents the hormone coming from the other phloem cells from being transported out of the cell with the help of the PAX regulator. The auxin which accumulates over time then leads to the degradation of BRX, causing the PAX regulator, which has now been activated, to export the auxin from the cell. Because the BRX protein is formed again with a certain time delay upon which it blocks auxin transport, the system regulates itself repeatedly like a rheostat.

"Many plant development processes are dependent on auxin transport and regulators similar to PAX. With the development of the negative regulation via the protein, a new control level has been discovered which could be just as applicable in other processes.

Comment: Another feedback loop control. Since they are circular, they require design to create the mechanism. A loop cannot design itself by chance and meet itself on the other side of the loop.

Genome complexity in embryology: control by electricity

by David Turell @, Friday, July 06, 2018, 19:20 (2093 days ago) @ David Turell

Bio-electric fields are shown to control embryological formations of tissues. The work is on brainless tadpoles:

https://www.quantamagazine.org/brainless-embryos-suggest-bioelectricity-guides-growth-2...

"In recent years, by working on tadpoles and other simple creatures, Levin’s laboratory has amassed evidence that the embryo is molded by bioelectrical signals, particularly ones that emanate from the young brain long before it is even a functional organ. Those results, if replicated in other organisms, may change our understanding of the roles of electrical phenomena and the nervous system in development, and perhaps more widely in biology.

“'Levin’s findings will shake some rigid orthodoxy in the field,” said Sui Huang, a molecular biologist at the Institute for Systems Biology. If Levin’s work holds up, Huang continued, “I think many developmental biologists will be stunned to see that the construction of the body plan is not due to local regulation of cells … but is centrally orchestrated by the brain.”

***

"But it’s not just the brain that uses bioelectric signaling — the whole body does. All cell membranes have embedded ion channels, protein pores that act as pathways for charged molecules, or ions. Differences between the number of ions inside and outside a cell result in an electric gradient — the cell’s resting potential. Vary this potential by opening or blocking the ion channels, and you change the signals transmitted to, from and among the cells all around. Neurons do this as well, but even faster: To communicate among themselves, they use molecules called neurotransmitters that are released at synapses in response to voltage spikes, and they send ultra-rapid electrical pulses over long distances along their axons, encoding information in the pulses’ pattern, to control muscle activity.

***

"In 2015, Levin, his postdoc Vaibhav Pai, and other collaborators showed experimentally that bioelectric signals from the body shape the development and patterning of the brain in its earliest stages. By changing the resting potential in the cells of tadpoles as far from the head as the gut, they appeared to disrupt the body’s “blueprint” for brain development. The resulting tadpoles’ brains were smaller or even nonexistent, and brain tissue grew where it shouldn’t.

***

"Herrera-Rincon and the rest of the team didn’t stop there. They wanted to see whether they could “rescue” the developing body from these defects by using bioelectricity to mimic the effect of a brain. They decided to express a specific ion channel called HCN2, which acts differently in various cells but is sensitive to their resting potential.

***

"To make embryos express it, the researchers injected messenger RNA for HCN2 into some frog egg cells just a couple of hours after they were fertilized. A day later they removed the embryos’ brains, and over the next few days, the cells of the embryo acquired novel electrical activity from the HCN2 in their membranes.

"The scientists found that this procedure rescued the brainless tadpoles from most of the usual defects. Because of the HCN2 it was as if the brain was still present, telling the body how to develop normally. It was amazing, Levin said, “to see how much rescue you can get just from very simple expression of this channel.” It was also, he added, the first clear evidence that the brain controls the development of the embryo via bioelectric cues.

***

"Although Levin’s work is gaining recognition, the emphasis he puts on electricity in development is far from universally accepted. Epigenetics and bioelectricity are important, but so are other layers of biology, Zhao said. “They work together to produce the biology we see.” More evidence is needed to shift the paradigm, he added. “We saw some amazing and mind-blowing results in this bioelectricity field, but the fundamental mechanisms are yet to be fully understood. I do not think we are there yet.”

"But Nuccitelli says that for many biologists, Levin is on to something. For example, he said, Levin’s success in inducing the growth of misplaced eyes in tadpoles simply by altering the ion flux through the local tissues “is an amazing demonstration of the power of biophysics to control pattern formation.”

***
"The passage of time and the efforts of others carrying on Levin’s work will help his cause, suggested David Stocum, a developmental biologist and dean emeritus at Indiana University-Purdue University Indianapolis. “In my view, his ideas will eventually be shown to be correct and generally accepted as an important part of the framework of developmental biology.'”

Comment: Developing a whole body from one fertilized cell is a stupendous job and obviously requires many mechanisms, and a designed process.

Genome complexity in embryology: bone manufacture

by David Turell @, Monday, August 27, 2018, 19:35 (2041 days ago) @ David Turell

Complex in forming in the fetus and when repairing fractures:

https://medicalxpress.com/news/2018-08-art-bone.html

Cell differentiation is a widely studied phenomenon forming the basis of all developmental processes including fetal growth and bone fracture healing. A series of recent studies indicates the emerging role of chondrocyte-to-osteoblast transdifferentiation during bone tissue formation, known as endochondral ossification (replacing cartilage with bone).

While transdifferentiation is not a new phenomenon and occurs when mature cells switch from one differentiated phenotype to another, new data have identified three models for chondrocyte (cartilage) to osteoblast (bone) transdifferentiation during fracture healing. Now writing in Bone Research, Patrick Aghajanian and Subburaman Mohan have dissected the three emerging models and categorized them to better understand the process of bone building. The new knowledge will allow bioengineers in regenerative medicine to advance the molecular basis of bone repair.

During typical cell differentiation, programmed cells progress along a specific lineage until they reach an endpoint of terminal differentiation and apoptosis. Transdifferentiation does not follow the preprogrammed path, switching instead from one mature phenotype to another. Prior to assessing the newly discovered mechanisms of chondrocyte-to-osteoblast transdifferentiation, the authors first reviewed the traditional mechanism of endochondral ossification.

The typical process of replacing cartilage with bone is divided into primary and secondary pathways, beginning with a template of rapidly proliferating immature chondrocytes that secrete a collagen matrix. In the primary process, chondrocytes undergo differentiation to form the bone matrix, facilitate bone forming cells (mesenchymal stromal cells) to enter the process and differentiate into osteoblasts/osteocytes during embryogenesis, while the chondrocytes themselves become hypertrophic to undergo apoptosis. The secondary process occurs similarly but post-natally, during which immature chondrocytes become hypertrophic and undergo apoptosis, and the vasculature invades to transport marrow, mesenchymal stem cells and osteoclast precursors to initiate bone formation at the center and extend peripherally.

***

While the exact cause for chondrocyte to osteoblast transdifferentiation is unknown, regulatory factors are necessary for that transition. Runx2 gene, for instance, is a master regulator of osteogenic fate, capable of transdifferentiating adipocytes, primary skeletal myoblasts, odontoblasts and vascular smooth muscle cells to osteogenic cell types. Studies with animal models are required to validate the contribution of various signaling pathways identified in in vitro studies during chondrocyte-to-osteoblast transdifferentiation.

Comment: Look at the diagrams to see the complexity. Not by chance.

Genome complexity in embryology: directing construction

by David Turell @, Monday, August 27, 2018, 19:43 (2041 days ago) @ David Turell

In this case legs:

https://phys.org/news/2018-08-fruit-flies-legs-molecular-mystery.html

"What do cancer and the growing legs of a fruit fly have in common? They can both be influenced by a single molecule, a protein that tends to call the shots inside of embryos as they develop into living, breathing animals. Present in virtually every creature on the planet, this protein goes by the name Epidermal Growth Factor Receptor protein, or EGFR.

"Now a team of neuroscientists at Columbia University has figured out how to tease apart the many roles EGFR plays in the body—challenging conventional wisdom in the process. They report their findings in PLOS Genetics.

***

"EGFR signaling is woven into the fabric of development. It guides the formation of many body parts and has been an intense area of research focus for decades. Indeed, EGFR is so critical to development that disruptions to its normal activity likely play a role in everything from developmental disorders to Alzheimer's disease to cancer.

***

"the Columbia team tried a new approach. They focused on the EGFR ligands' many enhancers: small stretches of DNA that govern the ligands' activity and trigger EGFR activity in a precise manner in different parts of the body.

"'If you think of EGFR signaling as a soundboard, like what you'd find in a recording studio, enhancers are similar to the soundboard's knobs and dials," said Dr. Mann. "Just like turning those dials up or down changes the output of soundboard, turning up or down individual enhancers changes the ligand expression and, therefore, the resulting activity of signals."

"In this paper, the researchers first located the specific enhancers of the EGFR ligands that guided the fly's leg development. They then switched off only those enhancers.

"'In this way, we've managed to eliminate one small aspect of EGFR activity, leaving the rest of the signaling largely intact," said Dr. Mann.

"When doing so, they saw that the growth of the fly leg was not guided by a single source, the way a morphogen would act. Instead, the researchers found that EGFR sent signals from multiple different sources, located at different parts of the developing leg—knowledge made possible by the scientists' focus on enhancers.

"Because EGFR exists throughout the animal kingdom, these findings in the fly can be applied to studies of EGFR disruptions related to disease, such as developmental disorders and cancer."

Comment: this complex system did not develop by chance.

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