https://www.quantamagazine.org/all-life-on-earth-today-descended-from-a-single-cell-mee...

"In 2024, Moody and a team of interdisciplinary researchers, including geologists, paleontologists, system modelers and phylogeneticists, combined their knowledge to build a probabilistic model that reconstructs modern life’s shared ancestor and estimates when it lived.

"The analysis sketched a surprisingly complex picture of the cell. LUCA lived off hydrogen gas and carbon dioxide, boasted a genome as large as that of some modern bacteria, and already had a rudimentary immune system, according to the study. Its genomic complexity, the authors argue, suggests that LUCA was one of many lineages — the rest now extinct — living about 4.2 billion years ago, a turbulent time relatively early in Earth’s history and long thought too harsh for life to flourish.

***

"Not all experts in the field agree, however. Some argue that a few hundred million years is not enough time for complex life to have evolved. The authors stress that their analysis is a first attempt to paint a fuller, admittedly fuzzy, picture of LUCA. “I fully expect and hope people prove us wrong in certain aspects,” said Moody, the paper’s lead author, especially if those new results offer a clearer view of the ancient ancestor of all life we know.

"It’s no small task to puzzle out the nature of an entity that lived so long ago on fragmentary, inferential evidence. Microscopic fossils can get researchers part of the way, but the oldest traces of life date to only around 3.5 billion years ago, likely long after LUCA lived. That leaves LUCA’s descendants for us to study. “The way to study LUCA is to compare the diversity of genes and physiologies and metabolisms today, and then work backward,” said Fournier, who was not involved in the new work.

***

"One way to isolate the signal from evolutionary noise is to select only genes and proteins that show little evidence of horizontal gene transfer. The most prominent analysis of this sort, from 2016, suggested that LUCA was a relatively simple entity(opens a new tab) that was only “half alive,” dependent on the geochemistry of hydrothermal vents for energy. However, such a conservative focus on only the most obviously shared genes and proteins could bias researchers, leading to a conception of LUCA that is too simple, Donoghue said.

"So, instead of a binary, in-or-out approach, Moody and his colleagues computed the probability that a given gene was present. By comparing the gene trees to the species trees, the researchers estimated rates of horizontal gene transfer, gene loss and other evolutionary processes that could muck up the picture. At the end of the process, they assigned each gene a probability of having been part of LUCA’s genome.

“'They’ve taken the best-practice approach for a single family and scaled it up,” Goldman said.

"The team identified 399 gene families with a high chance of having been in LUCA, a number roughly in line with the conservative 2016 analysis. By also integrating the probabilities of thousands of other gene families, they estimated that LUCA’s genome likely encoded about 2,600 proteins — making it similar in size to the genomes of some modern-day bacteria.

"Given what’s known about these proteins, “you get a picture of this fairly complex organism,” Moody said. LUCA likely existed without oxygen by converting carbon dioxide and hydrogen gas into energy. Those inputs might have come from nonliving sources, such as hydrothermal vents or atmospheric gases at the ocean’s surface.

"Alternatively, LUCA may have dined on the chemical waste of other creatures, suggesting that it was already part of a complex ecosystem with other microbes. The analysis can’t provide direct evidence of this possible ancient ecology, since traces of such lineages are long gone. But it’s unlikely that LUCA would have evolved complexity in isolation, the authors argue. Since its metabolism is consistent with both relying on and potentially supporting other microbes, LUCA was likely part of a broader ecosystem, from which its lineage was the sole survivor.

***

"From these genes, they estimated that LUCA lived about 4.2 billion years ago — roughly 300 million years after the moon was formed from the collision of a Mars-size planet with Earth. This was a tumultuous time in our planet’s history. It likely took 100 million or 200 million years at minimum for the planet to settle down enough to support life.

"If that timeline is right, life had only a couple hundred million years to emerge and become fairly complex. LUCA and its early descendants would also have survived a period once thought too harsh for life, when Earth was continually bombarded with asteroids.

***

"Not all scientists buy that LUCA is that old. “It’s very difficult to imagine that LUCA was living before 4 billion years ago,” said Patrick Forterre(opens a new tab), former head of microbiology at the Pasteur Institute, who co-organized the conference where the term “LUCA” was coined. He argues that Earth would have needed more time to cool down after the moon formed, and he is skeptical that we can accurately infer the pace of evolution at the time of LUCA."

Comment: this is not origin of life research but the implication of such an early start is amazing. This universe was prepared for life to appear quickly. With ecosystems forming early.

https://evolutionnews.org/2024/08/james-shapiro-intelligent-design-has-a-valid-point-wi...

"One article, by University of Chicago biologist James Shapiro, is titled, “Evolution Is Neither Random Accidents nor Divine Intervention: Biological Action Changes Genomes.” Shapiro provides a very nice review of various functions that have been discovered for transposable elements — a type of repetitive DNA that was once labeled “junk,” but which we now know is “needed for various aspects of genome function.” He writes:

"[R]epetitive DNA was labelled as “junk DNA,” “selfish DNA,” or “selfish genetic elements.” Richard Dawkins famously erected a widely popular philosophy of evolution on the basis of “The Selfish Gene” (1976).

"Today, we recognize that most of this repetitive DNA is made up of transposable elements and other repeats needed for various aspects of genome function, especially developmental regulatory networks controlling cellular differentiation. The repeats help guide the origin of cell lines that comprise distinctive tissues, say bone tissue versus nervous tissue. Both have the same DNA, yet each cell type expresses the genome in distinctive ways controlled by different DNA repeats.

***

"Support for evolution guided by divine intervention has a toehold in the quasi-scientific Intelligent Design (ID) movement, initiated by Michael Behe (“Darwin’s Black Box: The Biochemical Challenge to Evolution,” 1996) and carried on by members of the Discovery Institute and other creationist think tanks. The basic argument that ID theorists make is that natural selection of random hereditary changes cannot produce genomes capable of expressing all the intricate networked adaptations modern molecular biology has revealed to operate in living organisms. This conundrum is, in Behe’s words, “irreducible complexity.” Hence, the ID theorists posit a need for divine intervention.

"The ID argument has a valid point with regard to the explanatory limits of neo-Darwinism, still widely regarded as the only legitimate scientific explanation of evolution. ID falls down by assuming (as do mainstream evolutionists) that genome change occurs from outside the boundaries of life itself. Within the scientific community, there is agreement that the hereditary variation necessary for evolutionary change occurs by natural means. But significant difference exists between scientists about what constitutes “natural means.” (my bold)

"Shapiro is a great biologist who has offered many keen insights into the nature of genomic functioning. He’s clearly not an ID proponent and that is fine. I would disagree with his characterization of ID as a negative argument against evolution in favor of “divine intervention.”

"But he’s absolutely correct to note that neo-Darwinism struggles to account for the “intricate networked adaptations modern molecular biology has revealed to operate in living organisms.” And I appreciate his recognition that ID got this one right. Shapiro thinks that natural genetic engineering can account for many of this intricate complexity — and we in the ID movement are interested in seeing how far these mechanisms of pre-programmed evolution can take us.

"For my part, I think they might be useful for fine-tuning pre-existing functions — and may be involved in what Emily Reeves recently wrote about as “continuous environmental tracking.” But I’m skeptical that Dr. Shapiro’s model can account for much of the basic complexity of life. For the moment, I’m content to be grateful to him as a non-ID scientist who recognizes something ID has gotten right."

Comment: reproduced in toto. With a kudo for ID Shapiro then shows full supports for his theory.

https://www.sciencedaily.com/releases/2024/08/240809135927.htm

"Since the genetic code was first deciphered in the 1960s, our genes seemed like an open book. By reading and decoding our chromosomes as linear strings of letters, like sentences in a novel, we can identify the genes in our genome and learn why changes in a gene's code affect health.

"This linear rule of life was thought to govern all forms of life -- from humans down to bacteria.

But a new study by Columbia researchers shows that bacteria break that rule and can create free-floating and ephemeral genes, raising the possibility that similar genes exist outside of our own genome.

***

"'We now know that, at least in bacteria, there can be other instructions not preserved in the genome that are nonetheless essential for cell survival."

***

"The bacterial defense system Sternberg and Tang picked to explore is an odd one: The system involves a piece of RNA with unknown function and a reverse transcriptase, an enzyme that synthesizes DNA from an RNA template. The most common defense systems in bacteria cut or degrade incoming viral DNA, "so we were puzzled by the idea of defending the genome by DNA synthesis," Tang says.

"To learn how the odd defense works, Tang first created a new technique to identify the DNA produced by the reverse transcriptase. The DNA he found was long but repetitive, containing multiple copies of a short sequence within the defense system's RNA molecule.

"He then realized that this portion of the RNA molecule folds into a loop, and the reverse transcriptase travels numerous times around the loop to create the repetitive DNA. "It's like you were intending to photocopy a book, but the copier just started churning out the same page over and over again," Sternberg says.

***

"'This is when Stephen did some ingenious digging and found that the DNA molecule is a fully functioning, free-floating, transient gene," Sternberg says.

"The protein coded by this gene, the researchers found, is a critical part of the bacteria's antiviral defense system. Viral infection triggers production of the protein (dubbed Neo by the researchers), which prevents the virus from replicating and infecting neighboring cells.

***

"The lab is now using Tang's methods to look for human extrachromosomal genes produced by reverse transcriptases.

"Thousands of reverse transcriptase genes exist in the human genome and many have still undiscovered functions. "There is a significant gap to be filled that might reveal some more interesting biology," Sternberg says.

***

"The reverse transcriptase that creates Neo has certain properties that may make it a better option for genome editing in the lab and for creating new gene therapies. And more mysterious reverse transcriptases exist in bacteria that are waiting to be explored.

"'We think bacteria may have a treasure trove of reverse transcriptases that could be opportune starting points for new technologies once we understand how they work," Sternberg says."

Comment: We have evolved from bacteria. They are a good resource for genome research. There are many layers of genome controls yet to be discovered.

https://www.science.org/content/article/our-last-common-ancestor-lived-4-2-billion-year...

"The last ancestor shared by all living organisms was a microbe that lived 4.2 billion years ago, had a fairly large genome encoding some 2600 proteins, enjoyed a diet of hydrogen gas and carbon dioxide, and harbored a rudimentary immune system for fighting off viral invaders. That’s the conclusion of a new study that compared the genomes of a diverse range of 700 modern microbes and looked for commonalities to identify which features arose first. Although the analysis doesn’t reveal how life got its start, it suggests a complex cellular organism somewhat similar to modern microbes evolved only a few hundred million years after Earth’s formation.

***

"Moody and his colleagues have gone a step further. They focused on five sets of “paralog,” or duplicated, genes that were found in multiple bacteria and archaea, suggesting the doubling happened prior to LUCA’s split into those descendants. Tracking whether a mutation is in both copies of those genes or just one makes it easier to pin down the timing of their duplication and thus the ages of common ancestors, Moody says.

"In so doing, their analysis suggested LUCA lived some 4.2 billion years ago. “It’s maybe a little bit earlier than other estimates, but not much,” says Rika Anderson, an evolutionary microbiologist at Carleton College who was not involved with the work.

"To probe LUCA’s lifestyle like Martin did, Moody’s group tracked 57 “marker” genes across 350 bacteria and 350 archaea species to construct a tree of life. That’s an advance over Martin’s team, which tracked genes shared by at least two orders of bacteria and two orders of archaea, Moody says. His team then separately tracked the evolutionary patterns of individual genes and gene families of all the available genes in those bacteria and archaea cataloged in a commonly used genomic database. By comparing the evolutionary histories of individual genes with those of the species, they could better determine what genes were duplicated, lost, or underwent horizontal gene transfer. From that, they deduced what was present in LUCA.

“'It’s a more robust approach,” Anderson says. But Martin counters that despite this effort “they get exactly the same result, 8 years later.”

"Indeed, the U.K. team’s analysis suggested LUCA fueled itself on a diet of carbon dioxide (CO2) and H2, as Martin has found. But they also found evidence LUCA had a gene that could have protected it from ultraviolet light, which suggests the microbe might have lived in surface waters, where it could have captured CO2 and H2 from the atmosphere, rather than at deep-sea vents. Still, like Martin, they spotted the signature of an enzyme called reverse gyrase that is commonly found in thermophiles, which they acknowledge means LUCA could also have thrived around those vents.

"Moody also found something new: that LUCA likely had 19 CRISPR-Cas9 genes, an apparatus modern bacteria rely on to chop up the genetic material of viral invaders (and the inspiration for the versatile genome editor now used in many fields). “LUCA had this early immune system as a way of avoiding viruses,” Moody says.

"That thrills Kaçar, as it hints at a thriving ecosystem of microbes and pathogens that far back. Anderson is equally enthused, noting that CRISPR-Cas9 systems are “kind of sophisticated.” That means in only a few hundred million years, early life managed to evolve complex microbes whose interactions quickly settled into the scaffolding of a simple ecosystem—a feat that modern studies trying to depict the long-lost LUCA can’t yet explain."

Comment: only 300.000 years after Earth formation, and complex life appeared. Much too quick for random mutations doing the job. More evidence for design.

https://www.newscientist.com/article/2413791-a-bacterium-switches-from-prey-to-predator...

Growing up at a different temperature seems to transform common prey bacteria into predators, suggesting that bacterial ecology is more fluid than we thought.

Two species of bacteria appear to reverse which is predator and which is prey depending on the temperature. Just a small temperature change is enough to cause the switch.

"The soil bacteria Myxococcus xanthus is a social species that hunts in packs – it forms temporary, multicellular “swarms” of individuals that chemically tear apart and soak up nutrients from other microbes. And its prey includes Pseudomonas fluorescens, a bacterium common in both soil and water.

***

"...when P. fluorescens was reared at 32°C, M. xanthus destroyed most of the population within four days. But surprisingly, the P. fluorescens reared at 22°C “slaughtered M. xanthus to extinction”, Vasse and her colleagues wrote in the paper. They realised that cooler-reared P. fluorescens secreted a chemical compound that could degrade and destroy other bacteria.

"In addition, the team observed that P. fluorescens grew rapidly after wiping out M. xanthus. This means that it was probably consuming nutrients from, and thus preying on, its one-time predator.

“'[This research] challenges the idea of having ‘fixed’ roles within communities,” says Vasse. “They can change so fast, so easily and so radically. It’s very brutal.”

Comment: this study is no surprise to Dr. Shapiro. However, we should note, the species is still the same adapted species. Bacteria as free-living-alone organisms must have altered defenses they can bring into play.

https://phys.org/news/2024-01-reveals-unexpected-strategy-competition-bacteria.html

"Understanding how Gabija and other elements of bacterial defense systems look and work—along with the mechanisms that viruses known as phages use to overcome these defenses and infect bacteria—promises to illuminate broader aspects of immunity, including human immunity and immune responses to cancer.

"Already, the team has revealed an unexpected strategy that phages might use to neutralize Gabija in the evolutionary arms race between bacteria and phages.

"'This is the importance of basic science," said Kranzusch, senior author of the paper. "We're learning how cells defend against infection."

"Gabija is one of hundreds of defense systems found in bacteria. It is present in about 15% of all bacteria whose genes have been sequenced.

"'It's one of the most prevalent bacterial defense systems," said Antine, who is first author of the study. "Yet very little was known about how it works or how viruses that infect bacteria can evade the system."

***

"Gabija, she learned, is a very large complex. It is about one-quarter the size of the ribosome, which is a huge molecular machine that performs the incredible task of using information from RNA to make proteins.

"Antine also learned that Gabija is formed using the instructions from just two genes, GajA and GajB. GajA forms proteins that connect in groups of four to form the center of the structure. GajB forms proteins that connect to form the outer winglike portions of the structure.

***

"It isn't yet clear how this large complex recognizes and defeats the phage. But Antine and Kranzusch suspect that the complex recognizes a specific structure formed by phage DNA and then degrades it.

"'Gabija has exquisitely evolved to hunt and destroy a very particular target," said Kranzusch.

***

"...she found that the phage evolved DNA that encodes a very large protein that surrounds Gabija and inactivates it.

""The protein forms this huge web around the entire outside of the complex," said Kranzusch. "This evasion technique creates a massive complex. It was a surprising result that changes the way we think about how phages interact with these defense systems."

"Phages are often thought of as small and simple, but Kranzusch has found that that's not always true. The phages he and Antine are studying are large, with DNA that holds hundreds of genes.

"Phages are also considered entities rather than living organisms because they require a host cell to replicate. Yet they actively evolve and change under pressure from defense systems like Gabija.

"'They are complex and can evolve and adapt with their host. They shape evolution," said Kranzusch.

"For next steps, Antine will dive into the precise mechanisms Gabija uses to defeat phages. These mechanisms are the result each side finding new ways to defeat the other. The same kind of one-upmanship goes on in cancer, as tumor cells find increasingly clever ways to evade the immune system and cancer treatments.

"'There are parallels between immunity in human cells and in bacteria," says Antine. "We're interested in the diversity, the many ways that immune systems combat something that is actively evolving against it."

Comment: it seems cancer cells, phages and bacteria all can edit DNA. And humans are now editing DNA. The appearance of multicellularity has removed that ability in those organisms' cells.

https://www.sciencedirect.com/science/article/abs/pii/S2451945623004415

"Commensal and pathogenic bacteria continuously evolve to survive in diverse ecological niches by efficiently coordinating gene expression levels in their ever-changing environments. Regulation through the RNA transcript itself offers a faster and more cost-effective way to adapt than protein-based mechanisms and can be leveraged for diagnostic or antimicrobial purposes. However, RNA can fold into numerous intricate, not always functional structures that both expand and obscure the plethora of roles that regulatory RNAs serve within the cell. Here, we review the current knowledge of bacterial non-coding RNAs in relation to their folding pathways and interactions. We posit that co-transcriptional folding of these transcripts ultimately dictates their downstream functions. Elucidating the spatiotemporal folding of non-coding RNAs during transcription therefore provides invaluable insights into bacterial pathogeneses and predictive disease diagnostics. Finally, we discuss the implications of co-transcriptional folding and applications of RNAs for therapeutics and drug targets.

"In order to survive and thrive, bacteria must constantly tune their metabolism and overall gene expression to adjust to their ever-changing environment and ecological niches. Because of the competition between species, it is crucial for their survival that bacteria adapt quickly to transient nutritional resources as well as external threats such as antibiotics and toxins. (my bold)

***

"In bacteria, a single multi-subunit RNA polymerase (RNAP) enzyme is responsible for the synthesis of all RNA transcripts within the cell. The core enzyme forms a conserved architecture4 comprising all of the regulatory functions necessary for the efficient and accurate synthesis and folding of the transcripts during all phases of transcription, namely initiation, elongation, and termination. RNAP is subject to multiple types of regulatory processes that, in combination, determine the overall levels of expression of all genes.

***

"Maintaining a temporal balance between transcription progress, folding, and RNA functional action is key to the survival of bacteria. Slight changes in the timing of transcription (too fast or too slow) therefore can have deleterious effects, leading to competitive disadvantages or even loss of viability. Examining the importance of the relative timescales of transcription and RNA folding therefore will allow for a deeper and more nuanced understanding of critical biomolecular processes.

***

"ncRNAs have emerged as significant players in gene regulation in all domains of life, including bacteria. Unlike coding RNAs, which are translated into proteins, ncRNAs are not recruiting the ribosome for translation, but instead typically perform regulatory functions at the transcriptional or post-transcriptional level (Figure 1). There are diverse classes of ncRNAs, varying in length and structure, with roles encompassing regulation of basal gene expression, stress responses,

***

"ncRNAs fold co-transcriptionally into intricate structures on a rugged energy landscape
Whereas a plethora of ncRNAs such as sRNAs are thought to modulate gene expression at the post-transcriptional level, increasing evidence points toward a more complex regulation that operates during the transcription process itself. RNA molecules in general, and ncRNAs such as riboswitches in particular, are complex structures folded into unique three-dimensional shapes."

Comment: this is a clear expression of why bacteria can edit their DNA so precisely. Shapiro's work is not mentioned.

https://phys.org/news/2024-01-notorious-cell-subpopulation-key-antibiotic.html

"Antibiotic overuse can lead to antibiotic resistance, but classic antibiotic resistance might not completely explain why antibiotics sometimes fail. Sub-populations of bacteria called persister cells can survive in the presence of lethal doses of antibiotics for prolonged periods. Although persister cells have been intensively researched, evidence linking them to poor patient outcomes has been limited.

"Scientists led by UNC School of Medicine microbiologist Brian Conlon, Ph.D., and Duke School of Medicine infectious diseases fellow Josh Parsons, MD, Ph.D., have now shown that E. coli can evolve in patients to produce increased persister cells and this leads to increased survival to antibiotics.

***

"Using clinical E. coli bacteremia isolates—bacteria from the blood of patients—Conlon, first author Joshua Parsons, MD, Ph.D., an infectious diseases fellow at Duke University, and colleagues found that high-persister mutants evolved in patients. The researchers then documented a 100-fold increase in persisters in one such mutant when challenged with the exact antibiotic doctors had used to treat patients from which the E. coli had been isolated.

"The mutant bacteria showed no loss of fitness in a mouse infection model and displayed a 10-fold increase in survival following the antibiotic challenge.

"Importantly, Conlon said his team documented the infections and treatment protocols of patients who had been prescribed antibiotics to clear E. coli infections. Conlon said that classical antibiotic resistance was not responsible for the poor outcomes in patients who did not clear infection with antibiotics.

"'Because of this research, we think persister formation is likely a significant contributor to antibiotic treatment failure in patients," Conlon said. "Our research strongly suggests that persister formation is an important metric to consider when treating patients with antibiotics."

"He also said that researchers should develop techniques to identify mutants that are likely to respond poorly to antibiotics because such information would influence treatment choices or duration of treatment. Additionally, developing new therapeutic approaches to target and kill persisters may improve patient treatment outcomes."

Comment: Shapiro showed how bacteria can edit DNA for survival. This is a prime example.

From the article: https://www.pnas.org/doi/10.1073/pnas.2314514121

*In the relapsed E. coli strain with the greatest increase in persisters (100-fold relative to initial isolate), we determined that the increase was due to a loss-of-function mutation in the ptsI gene encoding Enzyme I of the phosphoenolpyruvate phosphotransferase system. The ptsI mutant was equally virulent in a murine bacteremia infection model but exhibited 10-fold increased survival to antibiotic treatment. This work addresses the controversy regarding the clinical relevance of persister formation by providing compelling data that not only do high-persister mutations arise during bloodstream infection in humans but also that these mutants display increased survival to antibiotic challenge in vivo." (my bold)

Comment: this fits Behe's thesis that most evolution of this type involves loss of function. To me this means evolution of major new species is over.

https://www.the-scientist.com/news-opinion/bacteria-go-dormant-to-survive-antibiotics-a...

"Infections that can’t be treated are a significant problem. To search for ways to fight this growing health threat, Peter Hill and his colleagues at Harvard Medical School teased apart how antibiotic tolerance and persistence arise. They recently reported in Cell Host & Microbe that tolerance comes from mutations in genes related to nutrient production while persistent bacteria activate a specific DNA repair pathway to survive. (my bold)

***

"To find out which mutations were responsible for tolerance, Hill’s team infected macrophages with a strain of Salmonella that causes recurrent diarrheal disease,3 induced tolerance by exposing them to antibiotics, and sequenced the genomes of the surviving bacteria. They found mutations that stopped the bacteria from making certain molecules essential for life. Bacteria that cannot make these compounds grow slowly, which causes them to survive in the face of antibiotics that target dividing cells. Because tolerant bacteria only grow in nutrient-rich environments, Hill saw that the tolerant Salmonella were sensitive to antibiotics once they moved to favorable conditions.

"Next, the team studied antibiotic persistence, which results from a phenotypic switch that temporarily slows or stops growth in a small portion of antibiotic-susceptible bacteria. Like the tolerant bugs, the persistent bacteria grew slowly, if at all, within macrophages treated with antibiotics. But the researchers found that persistent Salmonella came alive in the macrophages once they removed the antibiotic stress.

"Because persistence arises from a phenotypic shift rather than a mutation, Hill and his colleagues performed RNA-sequencing on the persisters to see how antibiotic treatment affected gene expression in this dormant population. They observed an increase in a stress response pathway that bacteria induce in response to DNA double-strand breaks (DSBs)—a common side effect of genome replication within hostile macrophages.

***

"Testing macrophages in a lab offers a lot of information, but Hill and his team wanted to know what happens during infections in the human body. They obtained patient samples of a similar Salmonella strain and sequenced the bacterial genomes. To their surprise, they did not identify any of the tolerance mutations that showed up in their cell culture experiments. Instead, the isolates’ growth in antibiotic-treated macrophages mimicked that of persistent bacteria; there was a subpopulation that was not as susceptible to antibiotics and had robust activation of the DNA repair response. (my bold)

“'The observation that clinical isolates seem to behave closer to the persisters in terms of the [DNA repair] response is very interesting,” Nathalie Balaban, a professor at the Hebrew University of Jerusalem who was not involved in this study, wrote in an email. “It would be also good to see whether [the clinical isolates] reinfect macrophages better.”

"Understanding the role of DNA repair in driving persistence and tolerance will help researchers develop other treatment strategies for bacterial infections. Blocking the DNA repair necessary for Salmonella survival in combination with antibiotic treatment may stop infection relapse and slow the development of antibiotic resistance."

Comment: a marvelous example of how bacteria manipulate their DNA to survive.

https://www.nature.com/articles/d41586-023-03937-z?utm_source=Live+Audience&utm_cam...

"Jacob West-Roberts, a computational biologist at the University of California (UC) Berkeley, was scouring microbial DNA sequences for giant genes and discovered what he thought was a whopper: a gene encoding a protein made up of 1,800 amino acids. The average protein has a few hundred.

“'Wait till you see this,” responded his PhD adviser, UC Berkeley environmental microbiologist Jillian Banfield, and pointed out proteins longer than 30,000 amino acids, already known from sequencing data.

"Their team has now found dozens of even bigger proteins, including what might be the longest ever: an 85,000-amino-acid behemoth. The mega-molecules could help an enigmatic group of environmental microorganisms to feed on other microbial cells, the researchers propose. They describe their findings in a preprint posted on bioRxiv1 last month.

“It’s a good study,” says Brian Hedlund, a microbiologist at the University of Nevada, Las Vegas. “They essentially doubled the size of the largest known predicted proteins from 40,000 to 85,000 amino acids, which are all insane.”

***

"Giant proteins were especially common in Omnitrophota, a bacterial phylum first discovered in Yellowstone National Park in the northern United States in the 1990s and now commonly found in environmental samples. In total, the researchers found 46 Omnitrophota genes encoding proteins longer than 30,000 amino acids, including the 85,804-amino-acid-colossus, which turned up in waste water. “They were just absolutely everywhere,” says West-Roberts.

***

"Genome sequencing identified a gene predicted to encode a protein nearly 40,000 amino acids long, and matching protein fragments turned up in a biochemical assay. Harder’s team might even have caught a glimpse of the giant in electron micrographs of the Omnitrophota cells, which seemed to show them attacking and devouring other bacteria and microbes called archaea.

***

"The AI predictions of the proteins’ structures revealed more cell-wall-binding regions, but also a big surprise: a very long tube-like apparatus unlike anything researchers have ever seen. This structure could be involved in delivering molecules to prey, or could attach to other cells before the host microbe devours them.

***

"The fact that giant proteins are so common in Omnitrophota is especially surprising because of the microbes’ tiny physical size, says Oleg Reva, a bioinformatician at the University of Pretoria in South Africa. The study shows that giant proteins are “sophisticated weapons wielded by the diminutive microbial hunters in their pursuit of bacterial and archaeal prey”, he adds.

"The discovery of genes encoding proteins as longer than 85,000 amino acids does not mean that the molecules exist in this state in cells, researchers say. One possibility is that the protein is chopped into smaller pieces after it’s made, and these portions take on a range of functions in cells. That could explain why Harder’s team was able to find only pieces of its giant protein. “Currently I don’t see experimental evidence that these large proteins exist,” Harder says.

"Many of the giant proteins contain protein-breaking enzymes called peptidases, which could chop the Goliaths down into Davids, West-Roberts and his team say. Firm answers might require researchers to grow Omnitrophota cells, something that only Harder’s team has managed to do so far. “All the others, they’re just imaginary,” says Harder. “There’s a lot of mystery to solve.'”

Comment: I carefully looked for a reference to Shapiro in all the references. None. A shame. I assume God helped with the DNA editing as the molecules are so large.

https://www.quantamagazine.org/evolving-bacteria-can-evade-barriers-to-peak-fitness-202...

"Over the course of the last hundred years, evolutionary biologists have used mathematical models and, increasingly, lab experiments with living organisms to explore how populations of all sizes can move through fitness landscapes (sometimes called adaptive landscapes). Now, in a study just published in Science, researchers have engineered more than a quarter-million versions of a common bacterium and plotted each strain’s performance to create one of the largest lab-built adaptive landscapes ever. It enabled them to ask: How hard is it to get from any given point to the peaks?

***

"As huge as the fitness landscape in Wagner’s new paper is, it shows only what the bacteria are capable of in a single specific environment. If the researchers changed any of the particulars — if they changed the dose of the antibiotic or raised the temperature, say — they would get a different landscape. So although the findings seem to suggest that most E. coli strains can evolve antibiotic resistance, that outcome might be either far less likely or far more likely in the real world. All that seems certain is that most strains probably aren’t irrevocably sabotaged by their own minor successes.

***

"Wagner and Papkou are hoping to explore other versions of the landscape in future work. Papkou notes that it is not possible to map every permutation of even a single gene comprehensively — the landscape would explode to astronomical size almost immediately. But with lab-built landscapes and theoretical models, it should still be possible today to begin exploring whether universal principles undergird how an evolving entity can change in response to its environment.

“'The bottom line is: It is pretty easy for Darwinian evolution to start in a suboptimal position and move by force of natural selection to a high fitness peak,” Papkou said. “It was pretty astonishing.'”

Comment: Shapiro all over again. Bacteria have a definite way to protect themselves by editing DNA. Why? They started life and have stayed around to contribute positively to so many aspects of life like our gut microbiome.

https://www.nature.com/articles/d41586-023-03473-w?utm_source=Live+Audience&utm_cam...

"Scientists have produced an infant ‘chimeric’ monkey by injecting a monkey embryo with stem cells from a genetically distinct donor embryo1. The resulting animal is the first live-born chimeric primate to have a high proportion of cells originating from donor stem cells.

***

"But the monkey chimaera had to be euthanized when it was only ten days old because of hypothermia and breathing difficulties, highlighting the need for further optimization of the approach and raising ethical concerns, say researchers.

"Scientists have long sought to make animal chimaeras using embryonic stem cells, which are derived from an embryo’s inner region and can develop into a wide variety of tissues. Such stem cells can be genetically edited before being added to a recipient embryo.

***

"Esteban and his colleagues created recipient embryos by collecting eggs from female cynomolgus monkeys (Macaca fascicularis) and fertilizing the eggs.

"Meanwhile, the researchers extracted embryonic stem cells from one-week-old cynomolgus embryos and genetically edited the cells to display a green fluorescent signal. To grow the stem cells in the laboratory, the team finetuned the nutrients and growth-promoting proteins in the liquid in which the stem cells were grown. They then injected up to 20 green embryonic stem cells into each of the recipient embryos, yielding 74 chimeric embryos with a strong fluorescent signal.

***

"The team found that, on average, 67% of the cells across the 26 tested tissues, including the brain, lungs and heart, were descendants of the donor stem cells. The highest level of chimerism was seen in the adrenal gland: the progeny of donor stem cells made up 92% of total cells.

"The low birth rate of chimeric monkeys and the poor health of the one survivor suggest that the donor embryonic stem cells did not perfectly match the developmental state of the recipient embryo, says reproductive biologist Zhen Liu at the Chinese Academy of Sciences in Shanghai. The team plans to optimize this in future, he adds.

“This work is both impressive and commendable,” says stem-cell biologist Irene Aksoy at the Stem-cell and Brain Research Institute in Lyon, France, who was not involved in the study.

"The method might be used to grow human organs in pig or non-human primate tissues, says developmental cell biologist Shoukhrat Mitalipov, director of the Oregon Health and Science University in Portland.

“'If we can delete the genes encoding for, say, the kidney, in a large animal such as a pig or primate, we could introduce human cells to produce that organ instead,” he says. But he adds that using human–animal chimaeras for organ collection, especially if human embryonic stem cells contribute to the nervous system, brain or reproductive cells, comes with many ethical concerns." (my bold)

Comment: it turns out, we are not yet God-like. Growing organs in surrogate animals is really God-like and ethically frightening. Can we guarantee perfection when God doesn't?

https://www.sciencemagazinedigital.org/sciencemagazine/library/item/10_november_2023/41...

"A 17-year project to craft a synthetic genome for yeast cells has reached a watershed. Researchers revealed this week in 10 new papers that they have created designer versions of all yeast chromosomes and incorporated almost half of them into cells that can survive and reproduce. “It’s a milestone we have been working on for a long time,” says geneticist Jef Boeke of NYU Langone Health, director of the project.

"Researchers have tinkered with the genomes of yeast and many other organisms using editing technologies such as CRISPR. But building a new version from the ground up opens the way to making bigger changes to an organism’s genome and delving deeper into its organization, function, and evolution.

***

"The researchers didn’t attempt to redesign the genome one nucleotide at a time. Instead, they revised the native yeast genome, adding thousands of modifications that simplify its structure, boost its stability, and make it easier to study. For instance, they carved out the transposons, itinerant stretches of DNA that can leap from location to location in the genome, disrupting DNA sequences.

"They also pruned the genome by excising many of the introns, segments of DNA that don’t code for portions of proteins. And to make the new yeast genome easier to manipulate in future experiments, the team included several hundred short DNA sequences that can prompt sections of chromosomes to rearrange.

"In most cases, the researchers left genes on their original chromosomes. But a team led by synthetic biologist Yizhi “Patrick” Cai of the University of Manchester, international director of the project, created a new, 17th chromosome to house yeast’s 275 tRNA genes. They code for RNA molecules that transport amino acids, the building blocks of proteins.

"Although tRNAs are essential for protein synthesis, their genes “are a lot of trouble for the genome,” Cai says, because “they are DNA damage hotspots” that can cause breaks. By isolating these disruptive genes on one chromosome, the researchers hoped to tame them. They found that yeast cells could survive and grow—albeit more slowly than unmodified cells—with this newfangled chromosome, they report in Cell. Synthetic biologist Paul Freemont of Imperial College London calls this work “a tour de force.”

***

"Boeke and colleagues repeatedly mated cells harboring different synthetic chromosomes, eventually producing yeast that contained six full-size synthetic chromosomes and a fragment of another, but not the extra tRNA chromosome.

"This yeast grew slower than normal because of some harmful genomic glitches, but after the researchers identified and corrected them, the strain grew about as fast as unaltered cells, the team reported in a second Cell paper. They then used a similar mating approach to add another synthetic chromosome, bringing the total to 7.5. In these cells, more than 50% of the DNA is synthetic. “We are more than halfway there,” Boeke says.

***

"The team is now working to integrate the remaining chromosomes into a yeast cell and correct any genomic problems that arise. Boeke expects a yeast with a fully synthetic genome to debut in about a year."

Comment: now we ae doing God's work, not speciating in a real sense. Remember we are using living material to do the editing, so our editing is secondhand. We do not know how genes really produce their results. We simply know what genes produce.

https://phys.org/news/2023-11-bacteria-virus-arms-rare-window-rapid.html

"Borin and Meyer set bacteria and viruses together in a closed laboratory flask—just two teaspoons large—to study coevolution in action. As viruses infect their bacterial neighbors, the bacteria evolve new defensive measures to repel the attacks. The viruses then counter these adaptations with their own evolutionary changes that work around the new defensive measures.

"In only three weeks, this accelerated arms race between bacteria (Escherichia coli) and viruses (bacteriophage, or "phage") results in several generations of evolutionary adaptations. The new findings, published in the journal Science, reveal the emergence of distinct evolutionary patterns.

"'In this study we show the power of evolution," said Meyer, an associate professor in the Department of Ecology, Behavior and Evolution. "We see how coevolution between bacteria and phage drive the emergence of a highly complicated ecological network. Evolution doesn't have to be slow and gradual as Darwin thought."

***

"As bacteria and viruses adapted to each other's presence over time, two prominent repeating patterns emerged. These included nestedness, a development in which narrow interactions between bacteria and virus specialists are "nested" within a broader range of generalist interactions; and modularity, in which interactions between species form modules within specialized groups, but not between groups.

"'We were amazed to discover that our evolution experiment in tiny flasks had recapitulated the complex patterns that had been previously observed between bacteria and viruses collected at regional and transoceanic scales," said Borin."

Comment: I looked at the article itself to see if Shapiro was mentioned in the text or in the references. Strange since this fits exactly with his finding that bacteria can actively edit their DNA.

DAVID: Support for Shapiro

https://www.quantamagazine.org/andreas-wagner-pursues-the-secrets-to-evolutionary-succe...

QUOTES: Mammals originated more than 100 million years before they first became successful. Evolution experimented with different mammalian life forms and ways of life, such as flying like bats or water living like otters, or tree living, and so forth. A lot of these originated and went extinct again. They were so unsuccessful that they actually had to be reinvented by evolution. That happened in some mammalian lineages multiple times before mammals became really successful.

"We see analogous phenomena in bees and other insects. So many, many different life forms were not very successful in the beginning and then became successful.”

DAVID: Simple live on-their-own bacteria and yeast must have these abilities to survive and then evolve into our complexity where only minor adaptations can occur. A designer God would naturally do this with simple organisms.

dhw: The quotes makes it abundantly clear that the authors are not confining their conclusions to simple organisms or to minor adaptations. You are right, this all provides support for Shapiro, and it could also provide support for other theories. Evolution does not “experiment” with anything. It’s not a being but a process. Nobody would say evolution has a conscious mind! And so we might justifiably regard this whole article as support for the theory that your God did the experimenting, or Shapiro’s intelligent cells (possibly invented by your God) did it. One theory which the diversity and constant comings and goings does not support is that of an all-powerful, all-knowing God setting out with the sole purpose of designing H. sapiens and his food.

Aagreed.

https://www.quantamagazine.org/andreas-wagner-pursues-the-secrets-to-evolutionary-succe...

QUOTES: Mammals originated more than 100 million years before they first became successful. Evolution experimented with different mammalian life forms and ways of life, such as flying like bats or water living like otters, or tree living, and so forth. A lot of these originated and went extinct again. They were so unsuccessful that they actually had to be reinvented by evolution. That happened in some mammalian lineages multiple times before mammals became really successful.

"We see analogous phenomena in bees and other insects. So many, many different life forms were not very successful in the beginning and then became successful.”

DAVID: Simple live on-their-own bacteria and yeast must have these abilities to survive and then evolve into our complexity where only minor adaptations can occur. A designer God would naturally do this with simple organisms.

The quotes makes it abundantly clear that the authors are not confining their conclusions to simple organisms or to minor adaptations. You are right, this all provides support for Shapiro, and it could also provide support for other theories. Evolution does not “experiment” with anything. It’s not a being but a process. Nobody would say evolution has a conscious mind! And so we might justifiably regard this whole article as support for the theory that your God did the experimenting, or Shapiro’s intelligent cells (possibly invented by your God) did it. One theory which the diversity and constant comings and goings does not support is that of an all-powerful, all-knowing God setting out with the sole purpose of designing H. sapiens and his food.

https://www.quantamagazine.org/andreas-wagner-pursues-the-secrets-to-evolutionary-succe...

"Quanta spoke to Wagner over the phone recently about his new book, evolution as exploration, and the grand patterns that underlie biology.

***

"...when the bacterium Escherichia coli enters the human intestinal tract, the environment contains oxygen. But as it gets deeper into the bowel, the environment starts to lack oxygen. E. coli needs to express different genes depending on whether oxygen is there or not.

"It turns out E. coli has evolved this anticipatory response where as soon as it enters the gastrointestinal tract, it starts to turn on the needed genes before it hits the anoxic zone. Its foresight might have evolved out of the thousands of millions of times it has gone through intestinal tracts: When it gets warm or the pH drops, or whatever it is, then it needs to turn on these genes, because soon it’s going to run out of oxygen.

"We wanted to find out whether you could evolve something like that in the laboratory. So we cycled yeast between different stressful environments. Once yeast went through the cycle multiple times, would they start to turn on the genes for handling oxidative stress [from too much reactive oxygen] before the oxidative stress hit? We found some evidence that they did.

***

"I study evolution...There have been many life forms that were not very successful by any standard when they originated. They didn’t radiate into hundreds of species, and they didn’t cover large areas of the planet’s surface. But wait long enough, and they became very successful.

"The best example is grasses. Today, grasses are one of the most successful families of organisms on the planet. They cover huge amounts of territory on most continents and have evolved enormous diversity, with about 10,000 very different species. They range in size from the tiny tufts of Antarctic grasses to huge bamboo forests in Asia. Grasses are old. We find grass pollen in fossilized dinosaur dung from 65 million years ago. But what’s quite remarkable is that when grasses originated and for many millions of years thereafter, they were just eking out a living at the margins of the biosphere. For that to change, they had to wait literally 40 million years for their spot in the sun.

"We see similar patterns in a lot of organisms. Mammals originated more than 100 million years before they first became successful. Evolution experimented with different mammalian life forms and ways of life, such as flying like bats or water living like otters, or tree living, and so forth. A lot of these originated and went extinct again. They were so unsuccessful that they actually had to be reinvented by evolution. That happened in some mammalian lineages multiple times before mammals became really successful.

"We see analogous phenomena in bees and other insects. So many, many different life forms were not very successful in the beginning and then became successful.

***

"It was when we found this kind of phenomenon in the lab that I became interested in it. We took E. coli and exposed them to an environment that contains a lot of an antibiotic called ampicillin. Most of them will die in the presence of that antibiotic. But bacteria are extremely rapid at evolving antibiotic resistance, so within a few weeks, they have absolutely no problem surviving high dosages of it.

"We were interested in other traits that these bacteria acquired as a byproduct of that evolutionary process. To find out what they might be, we exposed the bacteria to hundreds of other toxic environments containing other antibiotics or toxins such as heavy metals or solvents. We knew from previous work that in many of these environments, bacteria could not survive or survive very poorly.

"The important thing to realize is that these bacteria had encountered none of those environments before our experiments. But we found that in 20 or so of these environments, the bacteria could survive pretty well. It was remarkable that as a byproduct of evolution for one thing you get something else altogether. And not just one thing, but multiple viability traits.

"When we see a property that’s evolved in an organism, we have this reflex of thinking that it’s a product of natural selection, right? That at some point, the property was useful to the organism’s survival, and that’s why we see it today. But as these kinds of experiments show, that’s not necessarily the case at all.

[Quanta] "It could have been selection for something completely different."

"Exactly. It could just be a byproduct. And so it’s probably not prudent to always take an adaptationist or selectionist viewpoint. There may be a lot of traits that exist for no good reason at all. (my bold)

***

"It could seem almost like these bacteria are clairvoyant, you know? Like they anticipated that at some point they would need to be resistant against antibiotics when humanity came along, right? But there’s a very mundane explanation that has to do with these latent kinds of traits that we identified in experiments in the lab. So these traits really exist out in nature. They’re not just artifacts of experiments."

Comment: Simple live on-their-own bacteria and yeast must have these abilities to survive and then evolve into our complexity where only minor adaptations can occur. A designer God would naturally do this with simple organisms.

https://www.quantamagazine.org/even-synthetic-life-forms-with-a-tiny-genome-can-evolve-...

"Seven years ago, researchers showed that they could strip cells down to their barest fundamentals, creating a life form with the smallest genome that still allowed it to grow and divide in the lab. But in shedding half its genetic load, that “minimal” cell also lost some of the hardiness and adaptability that natural life evolved over billions of years. That left biologists wondering whether the reduction might have been a one-way trip: In pruning the cells down to their bare essentials, had they left the cells incapable of evolving because they could not survive a change in even one more gene?

"Now we have proof that even one of the weakest, simplest self-replicating organisms on the planet can adapt. During just 300 days of evolution in the lab, the generational equivalent of 40,000 human years, measly minimal cells regained all the fitness they had sacrificed, a team at Indiana University recently reported in the journal Nature. The researchers found that the cells responded to selection pressures about as well as the tiny bacteria from which they were derived. A second research group at the University of California, San Diego came to a similar conclusion independently in work that has been accepted for publication.

“'It turns out life, even such simple wimpy life as a minimal cell, is much more robust than we thought,” said Kate Adamala, a biochemist and assistant professor at the University of Minnesota who was not involved in either study. “You can throw rocks at it, and it’s still going to survive.” Even in a genome where every single gene serves a purpose, and a change would seemingly be detrimental, evolution molds organisms adaptively.

“'It’s a stunning achievement,” said Roseanna Zia, a physicist at the University of Missouri whose research aims to build a physics-based model of a minimal cell and who was not involved in the study. The new work showed that even without any genome resources to spare, she said, the minimal cells could increase their fitness with random changes in essential genes.

***

"They calculated that the original minimal cell had lost 53% of its relative fitness along with its nonessential genes. The minimization had “made the cell sick,” Lennon said. Yet by the end of the experiments, the minimal cells had evolved all that fitness back. They could go toe-to-toe against the ancestral bacteria.

“'That blew my mind,” said Anthony Vecchiarelli, a microbiologist at the University of Michigan who was not involved in the study. “You would think that if you have only essential genes, now you’ve really limited the amount of evolution that … can go in the positive direction.”

***

"When Lennon and Moger-Reischer adjusted for the relative fitness of the organisms, they found that the minimal cells evolved 39% faster than the synthetic M. mycoides bacteria from which they were derived.

***

"The researchers found that most of the beneficial mutations favored by natural selection in their experiments were in essential genes. But one critical mutation was in a nonessential gene called ftsZ, which codes for a protein that regulates cell division. When it mutated in M. mycoides, the bacterium grew 80% larger. Curiously, the same mutation in the minimal cell didn’t increase its size. That shows how mutations can have different functions depending on the cellular context, Lennon said. (my bold)

***

"'They observed a “fear-greed trade-off,” a tendency also seen in natural bacteria to evolve mutations in genes that will help it grow rather than mutations that would produce more DNA repair proteins to correct the errors." (my bold)

Comment: pure experimentation in a Shapiro mold. My first bold notes the use of natural selection to explain the issue, when we know bacteria can edit DNA, not natural selection. The second bold shows they recognized Shapiro's work.

dhw: Now transferred to More Miscellany PART TWO.

Answered there.