https://phys.org/news/2024-07-rna-junk-genes.html

The study provides a detailed map of the 3'UTR regions of RNA in C. elegans. 3'UTRs (untranslated regions) are segments of RNA involved in gene regulation.

***

Genes are segments of DNA that contain the blueprints for an astonishing diversity of life on Earth. However, part of the secret to this versatility lies not in the genes themselves but in how their effects are delicately fine-tuned. Genes provide the instructions for making proteins, which play essential roles in building and repairing cells and tissues, speeding up chemical reactions and defending the body against pathogens.

***

"Once genetic instructions are transcribed from DNA into messenger RNA (mRNA), specialized segments of the mRNA—the 3'UTRs—can regulate how the proteins are produced.

"3'UTRs are sections of RNA located at the end of a messenger RNA molecule. They help to govern how and when proteins are made by controlling the stability and efficiency of the mRNA. This regulation allows for dynamic responses to environmental changes and enables control over protein production, which is essential for adapting to various physiological needs.

"Initially, noncoding RNAs like 3'UTRs were regarded as nonessential genetic fragments because they themselves do not code for proteins. However, recent research reveals that they are crucial for modifying gene behavior and influencing mRNA stability, localization and translation efficiency. Translation refers to the process of converting RNA into proteins composed of sequences of amino acids.

"3'UTRs are an integral part of a sophisticated and highly adaptable system of checks and balances on protein production. Additionally, these RNA regulatory elements often contain binding sites for other elements responsible for protein regulation, including microRNAs and RNA-binding proteins. (my bold)

***

"The insights gained from the new study have far-reaching implications for human health. Problems with gene control can lead to diseases like cancer, diabetes and neurological disorders. By providing a detailed map of 3'UTRs and their regulatory elements, the research offers new insights that could lead to better treatments and therapies."

Comment: it is now obvious every bit of DNA is there for a reason. The very fine tight controls of protein production reeks of design. Trial and error cannot accomplish this mechanism.

https://evolutionnews.org/2023/11/the-new-post-junk-dna-paradigm-of-molecular-biology-r...

“'Another Class of Genes That Produce RNAs”
The main point of Mattick’s new paradigm is that in addition to protein-coding genes, there’s “another class of genes that produce RNAs.” These “RNA genes” perform many diverse functions, but primarily they “act as regulatory molecules to control gene expression and organise nuclear territories and cytoplasmic domains during ontogeny.” He summarizes the new paradigm this way:

"n simplified Kuhnian terms, the dominant paradigm in molecular biology since its foundation that “genes encode proteins and sequences that do not are mainly junk” should be replaced by “genes encode proteins and regulatory RNAs, the latter required for the epigenetic control of developmental trajectories”. RNA is not simply an intermediate between gene and protein, but a major player in gene regulation and a contributor to inheritance.

"These RNA genes have many functions but a large proportion entail gene regulation-related functions that fall within the category of epigenetics. Mattick identifies multiple types of RNAs that perform these important functions:

"Small regulatory RNAs (e.g., microRNAs) which regulate translation of proteins, regulate epigenetic process, and are also involved in alternative splicing.

"Long non-coding RNAs (called “lncRNAs”) which also influence gene expression by controlling transcription factors and transcription-splicing and also modulate many genetically variable traits. Some may even encode peptides.

"Transposable elements are important for gene structure and function, and gene regulatory networks.

"Overall these types of functional RNAs undergo much post-transcriptional editing and are important for brain function, and also can foster “transgenerational epigenetic inheritance.”

"Mattick has explained this new paradigm elsewhere as well. In a weighty academic book published earlier this year, RNA: The Epicenter of Genetic Information (Taylor & Francis), Mattick along with bioengineer Paulo Amaral argue that “the genomes of humans and other complex organisms are not full of junk.” They acknowledge that this is “contrary to long-held … dogmas of evolutionary theory.” Here’s the striking quote in full:

"While the story is still unfolding, we conclude that the genomes of humans and other complex organisms are not full of junk but rather are highly compact information suites that are largely devoted to the specification of regulatory RNAs. These RNAs drive the trajectories of differentiation and development, underpin brain function and convey transgenerational memory of experience, much of it contrary to long-held conceptions of genetic programming and the dogmas of evolutionary theory."

JOHN MATTICK AND PAULO AMARAL, RNA: THE EPICENTER OF GENETIC INFORMATION (CRC-TAYLOR & FRANCIS, 2023), P. VII.

Comment: it is not my intent to beat the subject to death. This article teaches us more about RNA's many functions.

https://onlinelibrary.wiley.com/doi/full/10.1002/bies.202300080

"Abstract
Thomas Kuhn described the progress of science as comprising occasional paradigm shifts separated by interludes of ‘normal science’. The paradigm that has held sway since the inception of molecular biology is that genes (mainly) encode proteins. In parallel, theoreticians posited that mutation is random, inferred that most of the genome in complex organisms is non-functional, and asserted that somatic information is not communicated to the germline. However, many anomalies appeared, particularly in plants and animals: the strange genetic phenomena of paramutation and transvection; introns; repetitive sequences; a complex epigenome; lack of scaling of (protein-coding) genes and increase in ‘noncoding’ sequences with developmental complexity; genetic loci termed ‘enhancers’ that control spatiotemporal gene expression patterns during development; and a plethora of ‘intergenic’, overlapping, antisense and intronic transcripts. These observations suggest that the original conception of genetic information was deficient and that most genes in complex organisms specify regulatory RNAs, some of which convey intergenerational information."

From evolution news: https://evolutionnews.org/2023/11/newly-paper-in-bioessays-recognizes-kuhnian-paradigm-...

"This brings us to the article recently published in BioEssays, written by John Mattick, an Australian molecular biologist and Professor of RNA Biology at the University of New South Wales, Sydney. I have no evidence that Mattick has any affinities with intelligent design — but he’s a prime example of a bold scientist who has embraced new theories that challenge the reigning paradigm. Mattick has been indefatigable in following the evidence where it leads regarding evidence of function for “junk DNA.” In part because of his work, biology today has experienced a paradigm shift away from the concept of junk DNA. In fact, Mattick’s new BioEssays article, “A Kuhnian revolution in molecular biology: Most genes in complex organisms express regulatory RNAs,” frames the revolution in thinking over junk DNA precisely in “Kuhnian paradigm shift” terms.

***

" Mattick describes the previously reigning “junk DNA” paradigm in biology as having come from “prevailing assumptions.” The assumptions hold that “‘genes’ encode proteins, that genetic information is transacted and regulated by proteins, and that there is no heritable communication between somatic and germ cells.” This view that genes encode proteins is a key part of the “central dogma” of biology. Of course, no one denies that genes encode proteins — Mattick’s point is that they can do much more than this. They can also encode RNAs and the evidence shows that many non-protein-coding sequences of DNA actually encode RNAs that perform many types of vital functions in the cell."

Comment: the whole concept of junk DNA was a direct result of early concepts, which were wrong. Mattick explains:

"[T]heoretical biologists were integrating Mendelian genetics with Darwinian evolution, leading in 1942 to the so-called Modern Synthesis, which made two primary claims: mutations are random and somatic mutations are not inherited. … In 1968 Kimura proposed the neutral theory of molecular evolution, which posited that “an appreciable fraction” of the genome was evolving independently of natural selection. In 1969, Nei concluded that, given the “high probability of accumulating … lethal mutations in duplicated genomes … it is to be expected that higher organisms carry a considerable number of nonfunctional genes (nonsense DNA) in their genome”, leading Ohno to promote the concept of “junk DNA”, also arguing that “in order not to be burdened with an unbearable mutation load, the necessary increase in the number of regulatory systems had to be compensated by simplification of each regulatory system”. [Emphasis in the original."]

Evolution news: " Against this backdrop — permeated with evolutionary thinking about the origin of the genome — the idea of junk DNA flourished and spread throughout the biology community."

Comment: it is about time.

https://qbi.uq.edu.au/article/2022/03/junk-dna-key-controlling-fear

"A piece of “junk DNA” could be the key to extinguishing fear-related memories for people struggling with post-traumatic stress disorder (PTSD) and phobia, according to a study from The University of Queensland.

"An international research project, led by the Queensland Brain Institute’s Associate Professor Timothy Bredy, discovered the new gene while investigating how the genome responds to traumatic experiences.

“'Until recently, scientists thought the majority of our genes were made up of junk DNA, which essentially didn’t do anything.” Dr Bredy said.

“'But when researchers began to explore these regions, they realised that most of the genome is active and transcribed.”

***

"A new gene, labelled ADRAM by the researchers, was found to not only act as a scaffold for molecules inside the cell, but also helped coordinate the formation of fear-extinction memory.

***

"Until now, there have been no studies devoted to understanding these genes, let alone how they might influence brain function in the context of learning and memory.

“Our findings suggest that long non-coding RNAs provide a bridge, linking dynamic environmental signals with the mechanisms that control the way our brains respond to fear,” Dr Bredy said.

“'With this new understanding of gene activity, we can now work towards developing tools to selectively target long non-coding RNAs in the brain that directly modify memory, and hopefully, develop a new therapy for PTSD and phobia.”

"This study was published in Cell Reports (doi.org/10.1016/j.celrep.2022.110546)"

Comment: it may be boring to have me produce more findings on what seemed to be 'junk' in DNA. However Larry Moran is publishing a book still claiming most of it is junk. He won't give up despite his lonely position. I think Dan Graur is still with him. What they realize is teh old Darwin theory is dead unless junk exists showing chance appearing useless mutations in the genome.

https://evolutionnews.org/2022/01/blast-from-the-past-eugenie-scotts-failed-prediction-...

"Humans have six copies of the beta-globin gene. Five produce beta-globin proteins, but the sixth, the pseudogene copy, has a premature stop codon (and other mutations) that prevent translation into a protein. In Scott’s telling this means that the pseudogene cannot have any function whatsoever. But molecular biology now knows that pseudogenes can produce transcripts which can regulate protein-coding versions of the same gene—and that’s exactly what the researchers propose is going on here.

***

"The beta-globin pseudogene’s inability to produce a translatable RNA transcript does not preclude it from being functional. The researchers argue the pseudogene HBBP1 works something like an on/off switch, regulating expression of protein-coding beta-globin genes. Here’s a lengthy quote from the paper:

"n the light of recent studies on the chromatin conformation of the β-globin cluster, we present evidence sustaining that the strong functional constraints underlying the decreased contemporary diversity at these two regions were not driven by protein function but instead are likely due to a regulatory role in ontogenic switches of gene expression. … Over the past years, the β-globin cluster has been regarded as a complex genetic system and a paradigm of gene expression regulation. More recently, a boost of studies on the β-globin cluster have contributed to a better understanding of the mechanisms underlying the regulation of each gene in the cluster.

***

"But there’s a lot more to this story. You’ll note that they “hypothesize” function based upon clear genetic evidence and knowledge of how gene regulation operates. The precise function of the HBBP1 pseudogene was confirmed and identified in a 2021 paper published in Developmental Cell titled “Genome-wide analysis of pseudogenes reveals HBBP1’s human-specific essentiality in erythropoiesis and implication in b-thalassemia.

"The 2021 paper was unmistakable in reporting the important function of this pseudogene, stating: “Pseudogenic HBBP1 confers human-specific essentiality in erythropoiesis.” Erythropoiesis is the process of producing red blood cells, and they report “human-specific indispensability of the HBBP1 transcript” in erythropoiesis and find “HBBP1 is essential for erythroid development and differentiation.”

***

"In conclusion, pseudogenes represent a new layer in the flow of genetic information. The highly integrative framework implemented in this study provides a prototype for determining the function of pseudogenes under normal and pathological conditions. Exploration of species-specific regulatory functions of pseudogenes or even studies of population-specific pseudogenes are expected to blossom in future.

"In other words, the “traditional view” that pseudogenes are “functionless evolutionary relics” has hindered research into understanding the true nature of pseudogenes. But now that we’re overcoming that old view, they expect studies elucidating specific functions of pseudogenes to “blossom” in the future.

"The implication of this story is that in their rush to oppose intelligent design, Darwin defenders like Eugenie Scott and Ken Miller not only made an argument that has turned out to be completely wrong. It may also have slowed the progress of science."

Comment: this is a review from non-ID source material. Who named pseudogenes? Darwinists!! Who named junk DNA? Darwinists!! Note current research, not done by IDers, is demolishing false conclusions by Darwin defenders. Almost all DNA is shown to function. Nothing seems accidental from chance mutations. With no evidence of chance, design emerges as required.

https://www.quantamagazine.org/the-complex-truth-about-junk-dna-20210901/

"Many mysteries still surround the issue of what noncoding DNA is, and whether it really is worthless junk or something more. Portions of it, at least, have turned out to be vitally important biologically. But even beyond the question of its functionality (or lack of it), researchers are beginning to appreciate how noncoding DNA can be a genetic resource for cells and a nursery where new genes can evolve.

"Abstractions navigates promising ideas in science and mathematics. Journey with us and join the conversation. “Slowly, slowly, slowly, the terminology of ‘junk DNA’ [has] started to die,” said Cristina Sisu, a geneticist at Brunel University London.

***

"Cells use some of their noncoding DNA to create a diverse menagerie of RNA molecules that regulate or assist with protein production in various ways. The catalog of these molecules keeps expanding, with small nuclear RNAs, microRNAs, small interfering RNAs and many more. Some are short segments, typically less than two dozen base pairs long, while others are an order of magnitude longer. Some exist as double strands or fold back on themselves in hairpin loops. But all of them can bind selectively to a target, such as a messenger RNA transcript, to either promote or inhibit its translation into protein.

***

"By far the biggest category of noncoding DNA in the genomes of humans and many other organisms consists of transposons, segments of DNA that can change their location within a genome. These “jumping genes” have a propensity to make many copies of themselves — sometimes hundreds of thousands — throughout the genome, says Seth Cheetham, a geneticist at the University of Queensland in Australia. Most prolific are the retrotransposons, which spread efficiently by making RNA copies of themselves that convert back into DNA at another place in the genome. About half of the human genome is made up of transposons; in some maize plants, that figure climbs to about 90%.

***

"One category of noncoding DNA that intrigues many scientists these days is the pseudogenes, which are usually viewed as the remnants of working genes that were accidentally duplicated and then degraded through mutation. As long as one copy of the original gene works, natural selection may exert little pressure to keep the redundant copy intact.

"Akin to broken genes, pseudogenes might seem like quintessential genomic junk. But Cheetham warns that some pseudogenes may not be “pseudo” at all. Many of them, he says, were presumed to be defective copies of recognized genes and labeled as pseudogenes without experimental evidence that they weren’t functional.

"Pseudogenes can also evolve new functions. “Sometimes they can actually control the activity of the gene from which they were copied,” Cheetham said, if their RNA is similar enough to that of the working gene to interact with it. Sisu notes that the discovery in 2010 that the PTENP1 pseudogene had found a second life as an RNA regulating tumor growth convinced many researchers to look more closely at pseudogene junk.

***

"But how much of this DNA therefore qualifies as true “junk” in the sense that it serves no useful purpose for a cell? This is hotly debated. In 2012, the Encyclopedia of DNA Elements (Encode) research project announced its findings that about 80% of the human genome seemed to be transcribed or otherwise biochemically active and might therefore be functional. However, this conclusion was widely disputed by scientists who pointed out that DNA can be transcribed for many reasons that have nothing to do with biological utility.

***

"In the future, researchers may be less and less inclined to describe any of the noncoding sequences as junk because there are so many other more precise ways of labeling them now. For Sisu, the field’s best way forward is to keep an open mind when assessing the eccentricities of noncoding DNA and RNA and their biological importance. People should “take a step back and realize that one person’s trash is another person’s treasure,” she said."

Comment: This is a carefully drawn article, but as I have presented here most non-coding DNA has some alternative function so the 80% estimate of function from ENCODE is reasonable. The argument about the importance pf 'junk' is that chance mutations in evolution should produce lots of junk. That is not true from this evidence, so that suggests DNA may be designed as I believe.

https://www.sciencedaily.com/releases/2021/07/210723105258.htm

"Researchers have recently identified a DNA region known as VNTR2-1 that appears to drive the activity of the telomerase gene, which has been shown to prevent aging in certain types of cells. Knowing how the telomerase gene is regulated and activated and why it is only active in certain cell types could someday be the key to understanding how humans age and how to stop the spread of cancer.

***

"Their finding is based on a series of experiments that found that deleting the DNA sequence from cancer cells -- both in a human cell line and in mice -- caused telomeres to shorten, cells to age, and tumors to stop growing. Subsequently, they conducted a study that looked at the length of the sequence in DNA samples taken from Caucasian and African American centenarians and control participants in the Georgia Centenarian Study, a study that followed a group of people aged 100 or above between 1988 and 2008. The researchers found that the length of the sequence ranged from as short as 53 repeats -- or copies -- of the DNA to as long as 160 repeats.

"'It varies a lot, and our study actually shows that the telomerase gene is more active in people with a longer sequence," Zhu said.

"Since very short sequences were found only in African American participants, they looked more closely at that group and found that there were relatively few centenarians with a short VNTR2-1 sequence as compared to control participants. However, Zhu said it was worth noting that having a shorter sequence does not necessarily mean your lifespan will be shorter, because it means the telomerase gene is less active and your telomere length may be shorter, which could make you less likely to develop cancer.

***

"Zhu noted that since African Americans have been in the United States for generations, many of them have Caucasian ancestors from whom they may have inherited some of this sequence. So as a next step, he and his team hope to be able to study the sequence in an African population."

Comment: just more evidence there is little 'junk DNA' in our genome. The African white difference shows our human variant types are really somewhat different.

https://journals.asm.org/doi/full/10.1128/JVI.02299-20

"Long disregarded as junk DNA or genomic dark matter, endogenous retroviruses (ERVs) have turned out to represent important components of the antiviral immune response. These remnants of once-infectious retroviruses not only regulate cellular immune activation, but may even directly target invading viral pathogens. In this Gem, we summarize mechanisms by which retroviral fossils protect us from viral infections. One focus will be on recent advances in the role of ERVs as regulators of antiviral gene expression.

***

"...we see that ERVs work to initiate immune responses to viruses in a variety of ways:

"(A) ERVs use “viral mimicry” where ERV-encoded long non-coding RNA (lncRNA) molecules bind with viral RNA to activate pattern recognition receptors (PRRs) which activate an immune response.

"(B) LncRNAs produced by ERVs can also induce expression of antiviral cytokines, creating a “positive feedback loop enhancing antiviral immune responses.”

"(C) Proteins encoded by ERV DNA can also enhance immune responses by binding with toll-like receptors.

"(D) ERV envelope proteins (called ENVs) are the outer layer of viruses which protects the genetic material inside. ENVs can bind to receptors which harmful viruses might use to enter host cells, blocking them from entering.

"(E) ENV proteins can enter viruses themselves and interfere with the viral life-cycle, inactivating viruses before they infect new host cells.

"(F) ERV proteins can also stop viruses by interfering with viral capsids that have already entered host cells.

'(G) Some ERVs that are neither transcribed nor translated can promote recombination which increases the number of host genes that can be used to target viruses. This is an evolutionary mechanism, but it could explain how ERVs can be a built-in designed mechanism to increase immune responses within a species.

"(H) There are also very important ERV functions for regulating gene expression, as ERVs can act as promoters, enhancers, or transcription start sites for gene expression. The article explains just how common this is:

"This cooption of regulatory elements is not a rare phenomenon, and it has been estimated that about 20% of all transcription factor binding sites in humans are found in HERVs and other transposable elements. In line with this, a meta-analysis of chromatin immunoprecipitation sequencing (ChIP-Seq) data sets identified about 800,000 transcription factor binding sites within HERVs.

"Intriguingly, almost 90% of all HERVs represent so-called solo LTRs [long terminal repeats, which can serve as binding sites to regulate gene expression]. These HERVs lost the prototypical retroviral genes gag, pol, and env due to homologous recombination of their flanking LTR sequences, leaving single LTR promoters in the genome. Due to their activation upon immune stimulation, ERV LTRs have already been termed “landing strips for inflammatory transcription factors” (90), and evidence for their role in regulating cellular immune responses is growing."

Comment: So it turns out viruses can also be good, not bad. My view is God has a reason for everything, and as yesterday's essay shows, we are innocent bystanders in the war of eat or be eaten.

https://evolutionnews.org/2021/05/noncoding-junk-dna-is-important-for-limb-formation/

"A 2021 article in Nature, “Non-coding deletions identify Maenli lncRNA as a limb-specific En1 regulator,” reports important new functions for non-coding or “junk” DNA that underlie limb formation.

***

"The technical paper in Nature describes the research. The investigators examined the chromosomes of people who had naturally occurring limb malformation, and found that these people had deletions of DNA encoding long non-coding RNA sequences (lncRNAs) from human chromosome 2. They deleted corresponding DNA sequences in mice and found similar “severe congenital limb malformation,” suggesting these lncRNA sequences are functionally important:

"Here we show that genetic ablation of a lncRNA locus on human chromosome 2 causes a severe congenital limb malformation. We identified homozygous 27–63-kilobase deletions located 300 kilobases upstream of the engrailed-1 gene (EN1) in patients with a complex limb malformation featuring mesomelic shortening, syndactyly and ventral nails (dorsal dimelia). Re-engineering of the human deletions in mice resulted in a complete loss of En1expression in the limb and a double dorsal-limb phenotype that recapitulates the human disease phenotype. Genome-wide transcriptome analysis in the developing mouse limb revealed a four-exon-long non-coding transcript within the deleted region, which we named Maenli. Functional dissection of the Maenli locus showed that its transcriptional activity is required for limb-specific En1 activation in cis, thereby fine-tuning the gene-regulatory networks controlling dorso-ventral polarity in the developing limb bud.

***

"In the era of whole-genome sequencing, the findings described here underscore the need for a systematic annotation and functional characterization of lncRNA loci to interpret and classify non-coding genetic variants. They highlight the importance of elucidating the complex diversity of lncRNA modes of action to assess their role in organ development and disease.

***

"Another 2021 article in Nature shows why it’s no longer tenable for evolutionists to hide behind such an argument from ignorance. The article explains that over 130,000 functional “genomic elements, previously called junk DNA” have now been discovered, highlighting how important these “junk” segments have turned out to be: (my bold)

"t is now appreciated that the majority of functional sequences in the human genome do not encode proteins. Rather, elements such as long non-coding RNAs, promoters, enhancers and countless gene-regulatory motifs work together to bring the genome to life. Variation in these regions does not alter proteins, but it can perturb the networks governing protein expression With the HGP draft in hand, the discovery of non-protein-coding elements exploded. So far, that growth has outstripped the discovery of protein-coding genes by a factor of five, and shows no signs of slowing. Likewise, the number of publications about such elements also grew in the period covered by our data set. For example, there are thousands of papers on non-coding RNAs, which regulate gene expression."

Comment: All of these discoveries show that most human complaints about God's 'bad' designs are as my bold shows, arguments from ignorance. Human judgement is not God's judgement. What seems bad must be proven bad to have any honest discussion about God and His works.

https://medicalxpress.com/news/2021-02-epigenomic-reveals-circuitry-human-disease.html

"Over the past two decades, it has become apparent that those noncoding stretches of DNA, originally thought to be "junk DNA," play critical roles in development and gene regulation. In a new study published today, a team of researchers from MIT has published the most comprehensive map yet of this noncoding DNA.

"This map provides in-depth annotation of epigenomic marks—modifications indicating which genes are turned on or off in different types of cells—across 833 tissues and cell types, a significant increase over what has been covered before. The researchers also identified groups of regulatory elements that control specific biological programs, and they uncovered candidate mechanisms of action for about 30,000 genetic variants linked to 540 specific traits.

***

"Layered atop the human genome—the sequence of nucleotides that makes up the genetic code—is the epigenome. The epigenome consists of chemical marks that help determine which genes are expressed at different times, and in different cells. These marks include histone modifications, DNA methylation, and how accessible a given stretch of DNA is.

***

"Since the final draft of the human genome was completed in 2003, researchers have performed thousands of genome-wide association studies (GWAS), revealing common genetic variants that predispose their carriers to a particular trait or disease.

"These studies have yielded about 120,000 variants, but only 7 percent of these are located within protein-coding genes, leaving 93 percent that lie in regions of noncoding DNA.

"How noncoding variants act is extremely difficult to resolve, however, for many reasons. First, genetic variants are inherited in blocks, making it difficult to pinpoint causal variants among dozens of variants in each disease-associated region. Moreover, noncoding variants can act at large distances, sometimes millions of nucleotides away, making it difficult to find their target gene of action. They are also extremely dynamic, making it difficult to know which tissue they act in. Lastly, understanding their upstream regulators remains an unsolved problem.

"In this study, the researchers were able to address these questions and provide candidate mechanistic insights for more than 30,000 of these noncoding GWAS variants. The researchers found that variants associated with the same trait tended to be enriched in specific tissues that are biologically relevant to the trait. For example, genetic variants linked to intelligence were found to be in noncoding regions active in the brain, while variants associated with cholesterol level are in regions active in the liver.

"The researchers also showed that some traits or diseases are affected by enhancers active in many different tissue types. For example, they found that genetic variants associated with coronary heart disease (CAD) were active in adipose tissue, coronary arteries, and the liver, among many other tissues."

Comment: This brings us back to errors where a disease happens, but much of it involves 'traits' which may not be bad. This system God designed for adaptation has both good and bad, as we interpret the results. Is God required to produce perfection?

https://www.sciencedaily.com/releases/2021/01/210104145943.htm

"new research reveals the discovery of a new cog in the circadian clock - a genome-wide regulatory layer made up of small chains of non-coding nucleotides known as micro RNAS (miRNAs).

***

"Formerly thought to be "junk DNA," miRNAs are now known to affect gene expression by preventing messenger RNA from making proteins. Past research has indicated miRNAs may have a role in the function of circadian clocks but determining which of the hundreds of miRNAs in the genome might be involved remained a problem.

"Kay and his team, led by Lili Zhou, a research associate in the Keck School's Department of Neurology, turned to the Genomics Institute of the Novartis Research Foundation (GNF) in San Diego which has created robots capable of high throughput experiments. Working with scientists at the institute, Zhou developed a high throughput screen for a robot to test the close to 1000 miRNAs by individually transferring them into cells the team had engineered to glow on and off, based on the cell's 24-hour circadian clock cycle.

"'The collaboration with GNF made it possible for us to conduct the first cell-based, genome-wide screening approach to systematically identify which of the hundreds of miRNAs might be the ones modulating circadian rhythms," said Zhou."

"'Much to our surprise," said Kay, "we discovered about 110 to 120 miRNAs that do this.'"

Comment: Most DNA is purposeful which means it developed from design rather than by chance. The 'junk theory' to support Darwinism is totally dead as this article demonstrates.

https://cosmosmagazine.com/nature/marine-life/sea-sponge-with-quite-a-story-to-tell/?ut...

"Many human traits, such as height and disease susceptibility, depend on genes that are encoded in our DNA. These genes are switched on and off and further fine-tuned by important but hard-to-find regions in the genome.

"A particularly important class of these regions are known as enhancers, which boost the likelihood that a particular gene will be activated. Trying to find enhancers based on the genome sequence alone is incredibly difficult, like finding a light switch in a dark room.

***

"In a new study published in Science, we found that humans, mice, zebrafish — and most likely the entire animal kingdom — share enhancer regions with a sea sponge that comes from the Great Barrier Reef. Because sea sponges and humans last shared a common ancestor more than 700 million years ago, this means the functional mechanism has been preserved across all this time.

***

"...we extracted enhancer DNA from the sea sponge and injected it into a single cell from a zebrafish embryo. We found that while the sea sponge enhancer sequences were very different from zebrafish enhancer sequences, they still worked: they successfully and consistently drove the expression of a fluorescent protein in certain types of zebrafish cells.

"Based on computational predictions, we also identified and tested similar enhancers from humans and mice, to show that these sequences drive the expression of a fluorescent protein in similar zebrafish cell types during development.

"We discovered that despite differences between the genetic sequences of sponges and humans due to millions of years of evolution, we could identify a similar set of genomic instructions that controls gene expression in both organisms.

"Our findings represent a fundamental discovery in understanding the connection between our genomes and our physical traits.

"The sections of DNA that are responsible for controlling gene expression are notoriously difficult to find, study and understand. Even though they make up a significant part of the human genome, researchers are only beginning to understand this genetic “dark matter”."

Comment: Complete proof of common descent, if we ever needed it. More junk DNA gone, and more complexity understood. Genes primarily code for protein but networks of other DNA regions perform lots of the organizational work making phenotypes and physiological systems..

https://www.sciencenews.org/article/essential-genes-fast-evolution-junk-dna-heterochrom...

"A new study in fruit flies may help solve that puzzle. It shows that some new genes quickly become crucial because they regulate a type of DNA called heterochromatin. Once considered “junk DNA,” heterochromatin actually performs many important jobs, including acting like a tightly guarded prison: It locks up “bad actor” genes, preventing them from turning on and doing damage.

"Heterochromatin is also one of the fastest-changing bits of DNA in the body, so the genes that regulate it have to adapt quickly just to keep up, evolutionary biologist Harmit Malik at the Fred Hutchinson Cancer Research Center in Seattle and his colleagues report.

“'The work is a milestone,” said Manyuan Long, an evolutionary biologist at the University of Chicago who was not involved in the research. “It is really amazing seeing such an important role the heterochromatin plays in gene evolution.”

***

"About a decade ago, researchers discovered that new genes don’t just confer new functions; some may actually be necessary for survival. In the fruit fly Drosophila melanogaster, as many as 30 percent of essential genes are “new,” with some arising as recently as 3 million years ago — a flash in evolutionary timescales. The discovery overturned a long-held belief that important genes don’t really change much over the course of evolution.

***

"The team found that one of the new essential genes, dubbed Nicknack, issues instructions for a protein that binds to heterochromatin, although the details remain unknown.

***

"They tested this theory by swapping the gene from D. simulans into the D. melanogaster fly, expecting that if the genes were the same, the trade would have no effect. But instead, the female files survived the swap just fine, but all the males died. Malik thinks the difference between the sexes has to do with heterochromatin: The Y chromosome contains a lot of it.

“'It’s as if [D.] simulans’ [Nicknack gene] comes in with its hand tied behind its back,” Malik says. “It’s good enough to do its function in female flies, but in male flies, where there is a huge block of heterochromatin, it can’t.” In other words, the gene from one species is no match for its counterpart in the other.

"The result suggests that in the 2.5 million years since the two species split, D. melanogaster evolved its own version of Nicknack. And because the swap adversely affected the males, with their abundance of heterochromatin in the Y chromosome, the researchers concluded that Nicknack must play some crucial role in regulating heterochromatin. And since heterochromatin evolves so rapidly, the Nicknack gene has to evolve rapidly too, so it doesn’t become obsolete."

Comment: This study suggests much support for my theory that God dabbles as evolution proceeds. And. of course, more 'junk DNA' disappears.

Another report also covers this study:

https://www.quantamagazine.org/scientists-find-vital-genes-evolving-in-genomes-junkyard...

To dig deeper into this puzzling result, Kasinathan looked for clues to the functions of Nicknack and Oddjob, two essential ZAD-ZNF genes that evolved quickly.

***
According to Malik, this explains why Oddjob and Nicknack evolve so rapidly: They have to adjust to the changing DNA environment of the heterochromatin to remain functional. In some ways, they are like the genes of the immune system, which change quickly to keep up with rapidly evolving pathogens in a kind of arms race. But in this case, Malik said, “It’s almost like an arms race happening in the genome, just to preserve an essential function.”

***

Species today face problems that their ancestors didn’t, and those new problems require new solutions. But “what if it’s actually the evolution of these heterochromatin sequences that created the need for this essential function first?” Malik asked.

“The essential function itself may not be conserved, and that’s a heretical concept,” he continued. “We’re not just saying that the essential genes are not conserved. We are actually saying that it’s possible that the essential functions are not conserved, because it’s all context-specific.” (My bold)

Kasinathan and Malik are now turning their attention to the other ZAD-ZNF transcription factors, many of which also localize to the heterochromatin. “This compartment of the genome that we basically ignored because it’s so gene-poor … is actually, at least for the ZAD-ZNFs, the answer to this paradox of young genes becoming essential,” Malik said.

“If you’re interested in centromere function, if you only look at the genes that are totally conserved across humans, yeast and flies, you could be missing really important genes that are potential therapeutic targets,” Malik said. “We’ve let our intuition and dogma kind of bias us to the point where we might be missing a lot of important biology.”

Comment: The bold suggest s God edits as necessary

https://phys.org/news/2020-11-sea-sponge-scientists-unravel-million-year-old.html

"Australian scientists have found that humans, and most likely the entire animal kingdom, share important genetic mechanisms with a jelly-like sea sponge that comes from the Great Barrier Reef.

"Published in Science today, the research reveals some elements of the human genome—an organism's complete set of DNA—are functioning in the same way as the prehistoric sea sponge. This mechanism—which drives gene expression, key to species diversity across the animal kingdom—has therefore been preserved across 700 million years of evolution.

***

"'We collected sea sponge samples from the Great Barrier Reef, near Herron Island. At the University of Queensland, we extracted DNA samples from the sea sponge and injected it into a single cell from a zebrafish embryo. Without harming the zebrafish, we then repeated the process at the Victor Chang Cardiac Research Institute with hundreds of embryos, inserting small DNA samples from humans and mice as well."

"Dr. Wong says despite a lack of similarity between the sponge and humans due to millions of years of evolution, the team identified a similar set of genomic instructions that controls gene expression in both organisms.

"We were blown away by the results," Dr. Wong says.

"According to scientists, the sections of DNA that are responsible for controlling gene expression are notoriously difficult to find, study and understand. Even though they make up a significant part of the human genome, researchers are only starting to understand this genetic "dark matter".

"'We are interested in an important class of these regions called 'enhancers'," Dr. Wong says.

"'Trying to find these regions based on the genome sequence alone is like looking for a light switch in a pitch-black room. And that's why, up to this point, there has not been a single example of a DNA sequence enhancer that has been found to be conserved across the animal kingdom.

"'We are still a long way from a clear understanding of how DNA precisely shapes morphology in health and disease but our work is an important step in that direction."

***

"The team focused on an ancient gene that is important in our nervous system but which also gave rise to a gene critical in heart development.'"

Comment: As usual the 'dark areas' of DNA are purposeful. I cannot image a designing God who created a bunch of useless DNA. God, as I view Him, is purely purposeful, and never shows frivolous human thoughts or desires.

https://phys.org/news/2020-08-clues-aging-junk-dna.html

"Tom LaRocca, an assistant professor in the Department of Health and Exercise Science and faculty member in the Columbine Heath Systems Center for Healthy Aging at CSU, led the study to investigate a growing body of evidence that repetitive elements—transposons and other sequences that occur in multiple copies in the human genome—may become active over time as we age.

***

"To carry out the study, the researchers began by analyzing an existing RNA sequencing dataset gathered from skin cells in healthy human subjects aged 1-94 years old. Just as the Human Genome Project of the 1990s sought to sequence and map the approximately 20,500 genes in human DNA, RNA sequencing can provide a map of the entire transcriptome in the cells under study. From that analysis, which was all computational, the researchers found that transcripts from most major types of repetitive elements were increased in older subjects.

"In a second wave of study, the researchers verified their initial findings by performing their own lab analyses on skin cells from a biobank. Using fluorescent microscopy, the researchers tagged the transcript of a specific transposon, Charlie5, to see how it fluctuates with the age of cells: the brighter the tag appears under the microscope, the more Charlie5 transcript is detectable.

"As hypothesized, skin cells from older adults revealed a marked accumulation of Charlie5 transcript compared to cells from younger individuals, showing that repetitive element RNAs appear to accumulate with age.

"While an important observation, the grander outcome of this study is that repetitive RNA transcripts might be linked with biological age, or the health of a person's cells, as opposed to chronological age in years.

***

"A link between repetitive element transcripts and biological age was further confirmed by studying skin cells from patients with Hutchinson-Gilford progeria syndrome (HGPS), a premature aging syndrome, and by studying an RNA-sequencing dataset from the roundworm Caenorhabditis elegans.

"Why might repetitive element transcripts increase with age? The researchers suspect that chromatin—the complex of DNA and protein in cells that typically represses repetitive elements from being expressed—might become disrupted, allowing for the transcription of repetitive elements.

"All in all, for a portion of the genome that scientists used to ignore, evidence is growing that noncoding RNAs and repetitive elements play vital roles in regulating the rest of the human genome, and in this case, as potentially targetable biomarkers of aging.

"'This is a really big chunk of the genome that, for the longest time, no one really knew what it did, so they just kind of assumed it was junk. But we're finding more and more that these noncoding regions might not only be doing something, but they might have actual health implications," Cavalier said."

Comment: As more and more DNA is found to function, the stronger the evidence for design.

https://www.nature.com/articles/d41586-020-02139-1

"Less than 2% of the human genome encodes proteins. A grand challenge for genomic sciences has been mapping the functional elements — the regions that determine the extent to which genes are expressed — in the remaining 98% of our DNA. The Encyclopedia of DNA Elements (ENCODE) project, among other large collaborative efforts, was established in 2003 to create a catalogue of these functional elements and to outline their roles in regulating gene expression. In nine papers in Nature5–13, the ENCODE consortium delivers the third phase of its valuable project.

***

"Highly occupied target regions have been described before, but — by analysing the patterns in which proteins co-assemble at these regions, and the DNA sequences to which they bind — Partridge et al. have provided the first comprehensive evidence to support a speculative model of HOT-region formation. Under this model, a set of anchor DNA sequences first recruit specific transcription factors. These proteins increase chromatin accessibility, then serve as a core around which other binding proteins aggregate in a manner that is independent of DNA sequence. This could happen through protein–protein interactions and chromatin loops, which might link together multiple distant CREs.

"To further understand how distant CREs work together, Grubert et al.9 mapped chromatin loops in 24 human cell types. They showed that differences in chromatin looping between cell types can affect gene expression, by changing which distant enhancer elements regulate a gene, and which sections of a gene are retained after transcription (a process called alternative splicing). Their most intriguing finding was that housekeeping genes (those involved in day-to-day cell maintenance) often interact with just a few enhancer elements, whereas many enhancers make contact with genes that cause disease if one of two copies is mutated. This implies that a simpler circuitry favours steady and constant expression, whereas more-complex circuitry is needed to safeguard the expression of ‘dosage-sensitive’ genes.

***

"This catalogue of RNA elements substantially expands our knowledge of the regulatory components encoded in the human genome. It should enable researchers to predict genetic variants that alter RNA processing, and will constitute an invaluable resource for research into how protein–RNA interactions are regulated.

"The third phase of the ENCODE project is a tour de force. But because many regulatory elements act only in specific cell types or at particular times, it is not possible to precisely assess the completeness of the encyclopedia. It would be interesting to see how the project might incorporate single-cell technologies to tease out spatio-temporal-specific elements and so to further unveil the fundamentals of gene regulation."

Comment: Little junk left. This highly complex review article of over 6,000 papers cannot be reproduced here. CRE's are highly specific regulatory loop areas in DNA. Log in to see the diagrams. Amazingly complex. Our small genome, producing amazingly complex us, had to have these many levels of control and modifications.

https://phys.org/news/2020-07-junk-dna-free-stem-cells.html

"NIH researchers report for the first time that ancient viral genes that were once considered "junk DNA" may play a role in this process. The article describes a series of preclinical experiments that showed how some human endogenous retrovirus (HERV-K) genes inscribed into chromosomes 12 and 19 may help control the differentiation, or maturation, of human stem cells into the trillions of neurons that are wired into our nervous systems.

"Over the course of evolution, the human genome has absorbed thousands of human endogenous retrovirus genes. As a result, nearly eight percent of the DNA that lines our chromosomes includes remnants of these genes. Although once thought to be inactive, or "junk", recent studies have shown that these genes may be involved in human embryonic development, the growth of some tumors, and nerve damage during multiple sclerosis. Previously, researchers in Dr. Nath's lab showed that amyotrophic lateral sclerosis (ALS) may be linked to activation of the HERV-K gene. In this study, led by Tongguang (David) Wang, M.D., Ph.D., staff scientist at NINDS, the team showed that deactivation of the gene may free stem cells to become neurons.

***

"Surprisingly, they found that the surfaces of the stem cells were lined with high levels of HERV-K, subtype HML-2, an envelope protein, that viruses often use to latch onto and infect cells. These proteins progressively disappeared as the cells were served two rounds of "cocktails." One round nudged the cells into an intermediate, neural stem cell state followed by a second round that pushed the cells into finally becoming neurons. The researchers sped up this process by turning off HERV-K, HML-2 genes in the stem cells or by treating the cells with antibodies against the HML-2 protein. In contrast, they delayed neural differentiation by artificially overloading the cells with the HML-2 genes. Finally, the team discovered that interactions on the stem cell surfaces between HML-2 and another immune cell protein called CD98HC may restrain differentiation by triggering internal chemical reactions that are known to control cell growth and tumors. In the future, the team plans to explore how HERV-K genes may shape the wiring of a nervous system."

Comment: So called 'junk' is not junk, yet again. Our newer abilities to study and tailor DNA had produced many surprises. Most DNA, even with added viral DNA appears to be quite useful. It has been noted here, in the past that, that viral DNA has contributed to the advance of evolution.

DAVID: I think Tony has given much of what He thinks right here. It seems he has just trashed natural selection, and I've said I don't think very much of it as having any value in any form of the theory such as expressed by dhw. But I hope Tony will pitch in a little more.

Tony has not mentioned the theory as expressed by Talbott, Shapiro and myself. I also hope we will hear more from him! Are you there, Tony?

QUOTE: "Evolutionists have already failed this burgeoning field by relegating RNAs they didn’t understand to the “genetic junk” bin. And ever since, after all these years of discovery, all they can do is speculate about what “might have evolutionary underpinnings.” This is a great time for design advocates to read the messages in RNA and find out what they are saying." (David’s bold)

David's comment: A typical ID article pointing out how the research in RNA has opened a huge field for new discoveries. As the last paragraph shows, ID design experts will have different interpretations of the 'facts'.

TONY: Well, he's not wrong. Evolutionary biologist did relegate what they didn't understand, and have thus spent decades being surprised. The reason that their 'surprise' is so telling is that a good scientific theory makes predictions, and you're only surprised when the predictions are wrong. The extreme level of complexity makes the entire prospect of random chance and natural selection relatively ludicrous, but then, the entire theory of evolution has too much of a strangle hold to be dislodged by something as inconvenient as facts or the scientific method. As theories go, it has been wrong a lot.... like a lot a lot.

dhw: On this website we have long since agreed that random chance as the source of all the complexities is “relatively ludicrous”. Natural selection in itself simply means that Nature will preserve whatever works, and will get rid of what doesn’t. What is ludicrous is the claim that it creates anything. Darwin’s “Origin of species by means of natural selection” is therefore horribly misleading, as his form of speciation depends initially on random mutations, not natural selection. However, none of this invalidates the theory of evolution itself in the sense of common descent, and indeed as Darwin says at the end of his book (later editions): “There is grandeur in the view of life, with its several powers, having been originally breathed by the Creator into a few forms or one.” For years now, we have been discussing the theory that evolution has advanced by means of cooperation between intelligent cell communities (as opposed to random mutations), possibly created by your God and responding in their different ways to different conditions. I don't remember hearing your views on this theory, but if you have told us, perhaps you could give us a reminder?

I think Tony has given much of what He thinks right here. It seems he has just trashed natural selection, and I've said I don't think very much of it as having any value in any form of the theory such as expressed by dhw. But I hope Tony will pitch in a little more.

David's comment: A typical ID article pointing out how the research in RNA has opened a huge field for new discoveries. As the last paragraph sows, ID design experts will have different interpretations of the 'facts'.

TONY: Well, he's not wrong. Evolutionary biologist did relegate what they didn't understand, and have thus spent decades being surprised. The reason that their 'surprise' is so telling is that a good scientific theory makes predictions, and you're only surprised when the predictions are wrong. The extreme level of complexity makes the entire prospect of random chance and natural selection relatively ludicrous, but then, the entire theory of evolution has too much of a strangle hold to be dislodged by something as inconvenient as facts or the scientific method. As theories go, it has been wrong a lot.... like a lot a lot.

On this website we have long since agreed that random chance as the source of all the complexities is “relatively ludicrous”. Natural selection in itself simply means that Nature will preserve whatever works, and will get rid of what doesn’t. What is ludicrous is the claim that it creates anything. Darwin’s “Origin of species by means of natural selection” is therefore horribly misleading, as his form of speciation depends initially on random mutations, not natural selection. However, none of this invalidates the theory of evolution itself in the sense of common descent, and indeed as Darwin says at the end of his book (later editions): “There is grandeur in the view of life, with its several powers, having been originally breathed by the Creator into a few forms or one.” For years now, we have been discussing the theory that evolution has advanced by means of cooperation between intelligent cell communities (as opposed to random mutations), possibly created by your God and responding in their different ways to different conditions. I don't remember hearing your views on this theory, but if you have told us, perhaps you could give us a reminder?