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Seeing Emergent Physics Behind Evolution

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Jordana Cepelewicz interviews Nigel Goldenfeld, director of the NASA Astrobiology Institute for Universal Biology.

The physicist Nigel Goldenfeld hates biology — “at least the way it was presented to me” when he was in school, he said. “It seemed to be a disconnected collection of facts. There was very little quantitation.” That sentiment may come as a surprise to anyone who glances over the myriad projects Goldenfeld’s lab is working on. He and his colleagues monitor the individual and swarm behaviors of honeybees, analyze biofilms, watch genes jump, assess diversity in ecosystems and probe the ecology of microbiomes. Goldenfeld himself is director of the NASA Astrobiology Institute for Universal Biology, and he spends most of his time not in the physics department at the University of Illinois but in his biology lab on the Urbana-Champaign campus.

Goldenfeld is one in a long list of physicists who have sought to make headway on questions in biology: In the 1930s Max Delbrück transformed the understanding of viruses; later, Erwin Schrödinger published What is Life? The Physical Aspect of the Living Cell; Francis Crick, a pioneer of X-ray crystallography, helped discover the structure of DNA. Goldenfeld wants to make use of his expertise in condensed matter theory, in which he models how patterns in dynamic physical systems evolve over time, to better understand diverse phenomena including turbulence, phase transitions, geological formations and financial markets. His interest in emergent states of matter has compelled him to explore one of biology’s greatest mysteries: the origins of life itself. And he’s only branched out from there. “Physicists can ask questions in a different way,” Goldenfeld said. “My motivation has always been to look for areas in biology where that kind of approach would be valued. But to be successful, you have to work with biologists and essentially become one yourself. You need both physics and biology.”

Quanta Magazine recently spoke with Goldenfeld about collective phenomena, expanding the Modern Synthesis model of evolution, and using quantitative and theoretical tools from physics to gain insights into mysteries surrounding early life on Earth and the interactions between cyanobacteria and predatory viruses. A condensed and edited version of that conversation follows.

Physics has an underlying conceptual framework, while biology does not. Are you trying to get at a universal theory of biology?

God, no. There’s no unified theory of biology. Evolution is the nearest thing you’re going to get to that. Biology is a product of evolution; there aren’t exceptions to the fact that life and its diversity came from evolution. You really have to understand evolution as a process to understand biology.

So how can collective effects in physics inform our understanding of evolution?

When you think about evolution, you typically tend to think about population genetics, the frequency of genes in a population. But if you look to the Last Universal Common Ancestor — the organism ancestral to all others, which we can trace through phylogenetics [the study of evolutionary relationships] — that’s not the beginning of life. There was definitely simpler life before that — life that didn’t even have genes, when there were no species. So we know that evolution is a much broader phenomenon than just population genetics.

The Last Universal Common Ancestor is dated to be about 3.8 billion years ago. The earth is 4.6 billion years old. Life went from zero to essentially the complexity of the modern cell in less than a billion years. In fact, probably a lot less: Since then, relatively little has happened in terms of the evolution of cellular architecture. So evolution was slow for the last 3.5 billion years, but very fast initially. Why did life evolve so fast?

[The late biophysicist] Carl Woese and I felt that it was because it evolved in a different way. The way life evolves in the present era is through vertical descent: You give your genes to your children, they give their genes to your grandchildren, and so on. Horizontal gene transfer gives genes to an organism that’s not related to you. It happens today in bacteria and other organisms, with genes that aren’t really so essential to the structure of the cell. Genes that give you resistance to antibiotics, for example — that’s why bacteria evolve defenses against drugs so quickly. But in the earlier phase of life, even the core machinery of the cell was transmitted horizontally. Life early on would have been a collective state, more of a community held together by gene exchange than simply the sum of a collection of individuals. There are many other well-known examples of collective states: for example, a bee colony or a flock of birds, where the collective seems to have its own identity and behavior, arising from the constituents and the ways that they communicate and respond to each other. Early life communicated through gene transfer.

How do you know?

Life could only have evolved as rapidly and optimally as it did if we assume this early network effect, rather than a [family] tree. We discovered about 10 years ago that this was the case with the genetic code, the rules that tell the cell which amino acids to use to make protein. Every organism on the planet has the same genetic code, with very minor perturbations. In the 1960s Carl was the first to have the idea that the genetic code we have is about as good as it could possibly be for minimizing errors. Even if you get the wrong amino acid — through a mutation, or because the cell’s translational machinery made a mistake — the genetic code specifies an amino acid that’s probably similar to the one you should have gotten. In that way, you’ve still got a chance that the protein you make will function, so the organism won’t die. David Haig [at Harvard University] and Laurence Hurst [at the University of Bath] were the first to show that this idea could be made quantitative through Monte Carlo simulation — they looked for which genetic code is most resilient against these kinds of errors. And the answer is: the one that we have. It’s really amazing, and not as well known as it should be.

Later, Carl and I, together with Kalin Vetsigian [at the University of Wisconsin-Madison], did a digital life simulation of communities of organisms with many synthetic, hypothetical genetic codes. We made computer virus models that mimicked living systems: They had a genome, expressed proteins, could replicate, experienced selection, and their fitness was a function of the proteins that they had. We found that it was not just their genomes that evolved. Their genetic code evolved, too. If you just have vertical evolution [between generations], the genetic code never becomes unique or optimal. But if you have this collective network effect, then the genetic code evolves rapidly and to a unique, optimal state, as we observe today.

So those findings, and the questions about how life could get this error-minimizing genetic code so quickly, suggest that we should see signatures of horizontal gene transfer earlier than the Last Universal Common Ancestor, for example. Sure enough, some of the enzymes that are associated with the cell’s translation machineries and gene expression show strong evidence of early horizontal gene transfers.

How have you been able to build on those findings?

Tommaso Biancalani [now at the Massachusetts Institute of Technology] and I discovered in the last year or so — and our paper on this has been accepted for publication — that life automatically shuts off the horizontal gene transfer once it has evolved enough complexity. When we simulate it, it basically shuts itself off on its own. . .

Continue reading.

I am coming to the conclusions that everything in biology happens the way it does because it has to happen that way, given the principle of least effort. Obviously, there are outside forces impinging on the biological world—for example, the asteroid impact near Yucatan some 64 million years ago—but life’s response to such events still follows the least-effort principle.

That may also apply to human culture and our daily lives.

Written by LeisureGuy

4 September 2017 at 3:00 pm

Posted in Evolution, Science

Alien lifeforms might be living right under our noses, but how can we find them

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Science has operated on the assumption that life on earth arose only once, and all current lifeforms are evolved from a single common ancestor. Sarah Scoles writes in Aeon about a search for alien life here on earth.

In the late 1670s, the Dutch scientist Antonie van Leeuwenhoek looked through a microscope at a drop of water and found a whole world. It was tiny; it was squirmy; it was full of weird body types; and it lived, invisibly, all around us. Humans were supposed to be the centre and purpose of the world, and these microscale ‘animalcules’ seemed to have no effect – visible or otherwise – on our existence, so why were they here? Now, we know that those animalcules are microbes and they actually rule our world. They make us sick, keep us healthy, decompose our waste, feed the bottom of our food chain, and make our oxygen. Human ignorance of them had no bearing on their significance, just as gravity was important before an apple dropped on Isaac Newton’s head.

We could be poised on another such philosophical precipice, about to discover a second important world hiding amid our own: alien life on our own planet. Today, scientists seek extraterrestrial microbes in geysers of chilled water shooting from Enceladus and in the ocean sloshing beneath the ice crust of Europa. They search for clues that beings once skittered around the formerly wet rocks of Mars. Telescopes peer into the atmospheres of distant exoplanets, hunting for signs of life. But perhaps these efforts are too far afield. If multiple lines of life bubbled up on Earth and evolved separately from our ancient ancestors, we could discover alien biology without leaving this planet.

The modern-day descendants of these ‘aliens’ might still be here, squirming around with van Leeuwenhoek’s microbes. Scientists call these hypothetical hangers-on the ‘shadow biosphere’. If a shadow biosphere were ever found, it would provide evidence that life isn’t a once-in-a-universe statistical accident. If biology can happen twice on one planet, it must have happened countless times on countless other planets. But most of our scientific methods are ill-equipped to discover a shadow biosphere. And that’s a problem, says Carol Cleland, the originator of the term and its biggest proponent.

The idea came to Cleland, a philosopher at the University of Colorado at Boulder, when she spent a sabbatical year at the Centro de Astrobiología in Spain. She was studying the scientists, who were studying microorganisms.

‘If you have a sample of soil,’ she asked them, ‘how will you recognise what’s in it?’ The scientists rattled off the usual answers: slide it under a microscope, put it in a Petri dish, make millions of DNA copies, catalogue the genes. But that party line disturbed Cleland. ‘You couldn’t detect anything that wasn’t almost identical to familiar Earth life,’ she said. Their methods assumed that all microbes have genetic material that works like ours. Isn’t it possible, Cleland wondered, that life arose more than once here? If so, organisms from a second (or third) genesis would never turn up in our tests, because our tests are only meant to turn up familiar life. ‘But these organisms, if they exist, would leave traces in the environment,’ Cleland says.

In 2007 in the journal Studies in History and Philosophy of Biological and Biomedical Sciences, Cleland wrote about just such a trace: desert varnish. It’s a strange sheen, like a hardened waterfall, that covers desert rocks all over the planet. The streaks run down rocks from the desert of El Azizia in Libya to Antartica’s Dry Valley. Desert varnish – into which people have scraped petroglyphs for thousands of years – appears layer by layer, growing only the width of a human hair each millennium. The varnish is replete with arsenic, iron and manganese, although the rocks it coats are not. No known geochemical or biological process can account for its ingredients. And yet there it is. Since that discovery, Cleland has urged scientists not to discount – but to seek out – such anomalies as the varnish, things that don’t quite seem to fit. Because maybe they don’t fit.

Science’s modern-day explorers have unearthed increasingly anomalous organisms that are technically ‘familiar life’ – familiar in that they do adhere to the Central Dogma of molecular biology which explains the flow of genetic information in a biological system. Toxitolerants can live in nuclear waste; acidophiles can live in battery acid; obligate anaerobes die in the presence of oxygen; thermophiles thrive around hot vents deep in the ocean. Life, as they say in the movie Jurassic Park, finds a way.

But even the most familiar forms of life can be difficult to find. According to the latest estimates, we’ve discovered just 14 per cent of the dogma-following species on the planet. Of those, we can make only 1 per cent grow in the lab. A shadow biosphere might help us understand why. ‘Although we have good theoretical reasons for believing that life could be at least modestly different … we don’t know how different it could be,’ Cleland wrote in the seminal paper ‘The Possibility of Alternative Microbial Life on Earth’ (2005), co-authored with the astrobiologist Shelley Copley, also of the University of Colorado at Boulder. Just as a hammer and a sledgehammer can both pound a nail, other chemical combinations could lead to organisms that grow, adapt, respond to stimuli, and reproduce – that live, in other words. But which chemicals? And how? To understand that requires going back to the beginning. . .

Continue reading.

Written by LeisureGuy

2 September 2017 at 11:21 am

Posted in Evolution, Science

This miracle weed killer was supposed to save farms. Instead, it’s devastating them.

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Caitlin Dewey reports in the Washington Post:

Clay Mayes slams on the brakes of his Chevy Silverado and jumps out with the engine running, yelling at a dogwood by the side of the dirt road as if it had said something insulting.

Its leaves curl downward and in on themselves like tiny, broken umbrellas. It’s the telltale mark of inadvertent exposure to a controversial herbicide called dicamba.

“This is crazy. Crazy!” shouts Mayes, a farm manager, gesticulating toward the shriveled canopy off Highway 61. “I just think if this keeps going on . . .”

“Everything’ll be dead,” says Brian Smith, his passenger.

The damage here in northeast Arkansas and across the Midwest — sickly soybeans, trees and other crops — has become emblematic of adeepening crisis in American agriculture.

Farmers are locked in an arms race between ever-stronger weeds and ever-stronger weed killers.

The dicamba system, approved for use for the first time this spring, was supposed to break the cycle and guarantee weed control in soybeans and cotton. The herbicide — used in combination with a genetically modified dicamba-resistant soybean — promises better control of unwanted plants such as pigweed, which has become resistant to common weed killers.

The problem, farmers and weed scientists say, is that dicamba has drifted from the fields where it was sprayed, damaging millions of acres of unprotected soybeans and other crops in what some are calling a man-made disaster. Critics say that the herbicide was approved by federal officials without enough data, particularly on the critical question of whether it could drift off target.

Government officials and manufacturers Monsanto and BASF deny the charge, saying the system worked as Congress designed it.

The backlash against dicamba has spurred lawsuits, state and federal investigations, and one argument that ended in a farmer’s shooting death and related murder charges.

“This should be a wake-up call,” said David Mortensen, a weed scientist at Pennsylvania State University. . .

Continue reading.

Later in the report:

According to a 2004 assessment, dicamba is 75 to 400 times more dangerous to off-target plants than the common weed killer glyphosate, even at very low doses. It is particularly toxic to soybeans — the very crop it was designed to protect — that haven’t been modified for resistance.

Written by LeisureGuy

29 August 2017 at 4:59 pm

The Secret To A Healthier Microbiome

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Michaeleen Doucleff reports at NPR:

The words “endangered species” often conjure up images of big exotic creatures. Think elephants, leopards and polar bears.

But there’s another of type of extinction that may be occurring, right now, inside our bodies.

Yes, I’m talking about the microbiome — that collection of bacteria in our intestines that influences everything from metabolism and the immune system to moods and behavior.

For the past few years, scientists around the world have been accumulating evidence that the Western lifestyle is altering our microbiome. Some species of bacteria are even disappearing to undetectable levels.

“Over time we are losing valuable members of our community,” says Justin Sonnenburg, a microbiologist at Stanford University, who has been studying the microbiome for more than a decade.

Now Sonnenburg and his team have evidence for why this microbial die-off is happening — and hints about what we can possibly do to reverse it.

The study, published Thursday in the journal Science, focuses on a group of hunter-gatherers in Tanzania, called Hadza.

Their diet consists almost entirely of food they find in the forest, including wild berries, fiber-rich tubers, honey and wild meat. They basically eat no processed food — or even food that comes from farms.

“They are a very special group of people,” Sonnenburg says. “There are only about 2,200 left and really only about 200 that exclusively adhere to hunting and gathering.”

Sonnenberg and his colleagues analyzed 350 stool samples from Hadza people taken over the course of about a year. They then compared the bacteria found in Hadza with those found in 17 other cultures around the world, including other hunter-gatherer communities in Venezuela and Peru and subsistence farmers in Malawi and Cameroon.

The trend was clear: The further away people’s diets are from a Western diet, the greater the variety of microbes they tend to have in their guts. And that includes bacteria that are missing from American guts.

“So whether it’s people in Africa, Papua New Guinea or South America, communities that live a traditional lifestyle have common gut microbes — ones that we all lack in the industrialized world,” Sonnenburg says.

In a way, the Western diet — low in fiber and high in refined sugars — is basically wiping out species of bacteria from our intestines.

That’s the conclusion Sonnenburg and his team reached after analyzing the Hadza microbiome at one stage of the yearlong study. But when they checked several months later, they uncovered a surprising twist: The composition of the microbiome fluctuated over time, depending on the season and what people were eating. And at one point, the composition started to look surprisingly similar to that of Westerners’ microbiome.

During the dry season, Hadza eat a lot of more meat — kind of like Westerners do. And their microbiome shifted as their diet changed. Some of the bacterial species that had been prevalent disappeared to undetectable levels, similar to what’s been observed in Westerners’ guts.

But then in wet season — when Hadza eat more berries and honey — these missing microbes returned, although the researchers are not really sure what’s in these foods that bring the microbes back.

“I think this finding is really exciting,” says Lawrence David, who studies the microbiome at Duke University. “It suggests the shifts in the microbiome seen in industrialized nations might not be permanent — that they might be reversible by changes in people’s diets.

“The finding supports the idea that the microbiome is plastic, depending on diet,” David adds.

Now the big question is: What’s the key dietary change that could bring the missing microbes back?

Lawrence thinks it could be cutting down on fat. “At a high level, it sounds like that,” he says, “because what changed in the Hadza’s diet was whether or not they were hunting versus foraging for berries or honey,” he says.

But Sonnenburg is placing his bets on another dietary component: fiber — which is avital food for the microbiome.

“We’re beginning to realize that people who eat more dietary fiber are actually feeding their gut microbiome,” Sonnenburg says.

Hadza consume a huge amount of fiber because throughout the year, they eat fiber-rich tubers and fruit from baobab trees. These staples give them about 100 to 150 grams of fiber each day. That’s equivalent to the fiber in 50 bowls of Cheerios — and 10 times more than many Americans eat. . .

Continue reading.

See also How Modern Life Depletes Our Gut Microbes. It begins:

Looks like many of us don’t have the right stomach for a paleodiet. Literally.

Two studies give us a glimpse into our ancestors’ microbiome — you know, those trillions of bacteria that live in the human gut.

And the take-home message of the studies is clear: Western diets and modern-day hygiene have wiped a few dozen species right out of our digestive tracts. One missing microbe helps metabolize carbohydrates. Other bygone bacteria act as prebiotics. And another communicates with our immune system. . .

As cultures around the world become more “Western,” they lose bacteria species in their guts, Dominguez-Bello says. At the same time, they start having higher incidences of chronic illnesses connected to the immune system, such as allergies, Crohn’s disease, autoimmune disorders and multiple sclerosis.

“So the big question is: Are these two facts related?” Dominguez-Bello asks. “It’s not clear if more diversity in the microbiome is healthier. But maybe we have lost species with important functions.” . . .

Written by LeisureGuy

27 August 2017 at 11:18 am

The Fairy Tales That Predate Christianity

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Meme fans will immediately recognize the description that opens this Atlantic article by Ed Yong:

Stories evolve. As they are told and retold to new audiences, they accumulate changes in plot, characters, and settings. They behave a lot like living organisms, which build up mutations in the genes that they pass to successive generations.

This is more than a metaphor. It means that scientists can reconstruct the relationships between versions of a story using the same tools that evolutionary biologists use to study species. They can compare different versions of the same tale and draw family trees—phylogenies—that unite them. They can even reconstruct the last common ancestor of a group of stories.

In 2013, Jamie Tehrani from Durham University did this for Little Red Riding Hood, charting the relationships between 58 different versions of the tale. In some, a huntsman rescues the girl; in others, she does it herself. But all these iterations could be traced back to a single origin, 2,000 years ago, somewhere between Europe and the Middle East. And East Asian versions (with several girls, and a tiger or leopard in lieu of wolf) probably derived from these European ancestors.

That project stoked Tehrani’s interest, and so he teamed up with Sara Graça da Silva, who studies intersections between evolution and literature, to piece together the origins of a wider corpus of folktales. The duo relied on the Aarne Thompson Uther Index—an immense catalogue that classifies folktales into over 2,000 tiered categories. (For example, Tales of Magic (300-749) contains Supernatural Adversaries (300-399), which contains Little Red Riding Hood (333), Rapunzel (310), and more amusing titles like Godfather Death (332) and Magnet Mountain Attracts Everything (322).

Tehrani and da Silva recorded the presence of each Tales of Magic to 50 Indo-European populations, and used these maps to reconstruct the stories’ evolutionary relationships. They were successful for 76 of the 275 tales, tracing their ancestries back by hundreds or thousands of years. These results vindicate a view espoused by no less a teller of stories than Wilhelm Grimm—half of the fraternal duo whose names are almost synonymous with fairy tales. He and his brother Jacob were assembling German peasant tales at a time of great advances in linguistics. Researchers were unmasking the commonalities between Indo-European languages (which include English, Spanish, Hindi, Russian, and German), and positing that those tongues shared a common ancestor. In 1884, the Grimms suggested that the same applied to oral traditions like folktales. Those they compiled were part of a grand cultural tradition that stretched from Scandinavia to South Asia, and many were probably thousands of years old.

Many folklorists disagreed. Some have claimed that many classic fairy tales are recent inventions that followed the advent of mass-printed literature. Others noted that human stories, unlike human genes, aren’t just passed down vertically through generations, but horizontally within generations. “They’re passed across societies through trade, exchange, migration, and conquest,” says Tehrani. “The consensus was that these processes would have destroyed any deep signatures of descent from ancient ancestral populations.”

Not so. Tehrani and da Silva found that although neighboring cultures can easily exchange stories, they also often reject the tales of their neighbors. Several stories were less likely to appear in one population if they were told within an adjacent one.

Meanwhile, a quarter of the Tales of Magic showed clear signatures of shared descent from ancient ancestors. “Most people would assume that folktales are rapidly changing and easily exchanged between social groups,” says Simon Greenhill from the Australian National University. “But this shows that many tales are actually surprisingly stable over time and seem to track population history well.” Similarly, a recent study found that flood “myths” among Aboriginal Australians can be traced back to real sea level rises 7,000 years ago. . .

Continue reading.

See also this article.

Written by LeisureGuy

24 August 2017 at 6:34 pm

Posted in Books, Evolution, Memes, Science

Antarctic mystery microbe could tell us where viruses came from

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A fascinating report by Michael Marshall in New Scientist:

A peculiar Antarctic microbe may offer a clue to one of the biggest mysteries in evolution: the origin of viruses.

The microorganism is host to a fragment of DNA that can build a capsule around itself. It may help solve the mystery of how viruses first arose.

Viruses are not like other life forms. Arguably, they are not alive at all. All other living things are made of cells: squashy bags filled with the other essential molecules of life. Cells are intricate machines that can feed and reproduce independently.

Viruses are much simpler. A typical virus is a small piece of genetic material encased in a shell called a capsid. On its own, a virus can do little. But if it enters a living cell, it starts making copies of itself. Viruses often harm their hosts: for instance, the human immunodeficiency virus (HIV) can cause AIDS when it infects a person.

Biologists have puzzled for decades about where viruses come from. Are they an older, simpler form of life – or are they parasites that arose only once cells had evolved?

Blurred lines

Ricardo Cavicchioli of the University of New South Wales in Australia and his colleagues have found a microorganism in the lakes of the Rauer Islands off the coast of Antarctica that might shed some light on the question. The organism, which they named Halorubrum lacusprofundi R1S1, is an archaean: a kind of single-celled organism that looks like a bacterium, but actually belongs to a separate domain of life.

The group knew that viruses often play an important role in Antarctic ecosystems, so team member Susanne Erdmann searched for viruses inside the organism’s cells. She found something unexpected: a plasmid.

Plasmids are small fragments of DNA, often circular, that reside in living cells. They are not part of the cell’s main genome, and can replicate themselves independently. Often, a plasmid will carry a gene that is somehow useful to the cell: for instance, antibiotic resistance genes are sometimes found on plasmids.

The plasmid Erdmann found, which the team calls “pR1SE”, is unusual. The genes it carries allow it to make vesicles – essentially bubbles made of lipids – that enclose it in a protective layer. Encased in its protective bubble, pR1SE can leave its host cell to seek out new hosts.

In other words, pR1SE looks and acts a lot like a virus. But it carries genes that are found only on plasmids, and lacks any telltale virus genes. It is a plasmid with the attributes of a virus. “There really are no major distinctions left between plasmids and viruses,” says Cavicchioli.

Escaping genes

He suggests that viruses could have evolved from plasmids like pR1SE, by acquiring genes from their host that allowed them to make a hard capsid shell rather than a soft vesicle.

This lines up with existing evidence on the origin of viruses.

There have been three leading ideas: . . .

Continue reading.

Written by LeisureGuy

22 August 2017 at 9:50 am

Posted in Evolution, Science

Beating the Odds for Lucky Mutations

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Jordana Cepelewicz writes in Quanta:

In 1944, a Columbia University doctoral student in genetics named Evelyn Witkin made a lucky mistake. During her first experiment in a laboratory at Cold Spring Harbor, in New York, she accidentally irradiated millions of E. coli with a lethal dose of ultraviolet light. When she returned the following day to check on the samples, they were all dead — except for one, in which four bacterial cells had survived and continued to grow. Somehow, those cells were resistant to UV radiation. To Witkin, it seemed like a remarkably lucky coincidence that any cells in the culture had emerged with precisely the mutation they needed to survive — so much so that she questioned whether it was a coincidence at all.

For the next two decades, Witkin sought to understand how and why these mutants had emerged. Her research led her to what is now known as the SOS response, a DNA repair mechanism that bacteria employ when their genomes are damaged, during which dozens of genes become active and the rate of mutation goes up. Those extra mutations are more often detrimental than beneficial, but they enable adaptations, such as the development of resistance to UV or antibiotics.

The question that has tormented some evolutionary biologists ever since is whether nature favored this arrangement. Is the upsurge in mutations merely a secondary consequence of a repair process inherently prone to error? Or, as some researchers claim, is the increase in the mutation rate itself an evolved adaptation, one that helps bacteria evolve advantageous traits more quickly in stressful environments?

The scientific challenge has not just been to demonstrate convincingly that harsh environments cause nonrandom mutations. It has also been to find a plausible mechanism consistent with the rest of molecular biology that could make lucky mutations more likely. Waves of studies in bacteria and more complex organisms have sought those answers for decades.

The latest and perhaps best answer — for explaining some kinds of mutations, anyway — has emerged from studies of yeast, as reported in June in PLOS Biology. A team led by Jonathan Houseley, a specialist in molecular biology and genetics at the Babraham Institute in Cambridge, proposed a mechanism that drives more mutation specifically in regions of the yeast genome where it could be most adaptive.

“It’s a totally new way that the environment can have an impact on the genome to allow adaptation in response to need. It is one of the most directed processes we’ve seen yet,” said Philip Hastings, professor of molecular and human genetics at Baylor College of Medicine, who was not involved in the Houseley group’s experiments. Other scientists contacted for this story also praised the work, though most cautioned that much about the controversial idea was still speculative and needed more support.

Increasing Variety in the Genome

“Rather than asking very broad questions like ‘are mutations always random?’ I wanted to take a more mechanistic approach,” Houseley said. He and his colleagues directed their attention to a specific kind of mutation called  . . .

Continue reading.

Written by LeisureGuy

16 August 2017 at 2:23 pm

Posted in Evolution, Science

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