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Archive for the ‘Evolution’ Category

We find a new way that viruses hijack cells

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Veronique Greenwood reports in Quanta:

ruses travel light. Most carry just their genetic material and a few tools to break into the cells of their hosts — after that, they hijack the host’s own machinery to manufacture thousands of copies of themselves. In recent decades, biologists have gained a clearer picture of just how this heist is pulled off. Many viruses, it turns out, suppress the messages that cells send to control their daily operations. This information interference shuts down some cellular functions that the attacking virus doesn’t need, and boosts others.

But some viruses do something more subtle and complex, as biologists at the University of California, San Diego, reported recently. The scientists looked at cells infected with cytomegalovirus, a common cause of birth defects. CMV infection doesn’t block cellular messages; instead, it changes their content, the team found. In a new paper in Nature Structural and Molecular Biology, they detail thousands of changes in these host communications, which may be the virus whispering sedition to remodel the cell.

To understand the importance of what is going on here, first consider how the cell functions normally. At the heart of the whole affair is the DNA — a sort of code book of instructions for how to make everything in the cell — which is kept under lock and key in the nucleus. When the cell needs to manufacture a protein, the relevant portion of the DNA is transcribed. That transcript, called a messenger RNA, leaves the nucleus and heads to the machinery that will use it as a template to make the new protein.

But along the way, the RNA can be edited in a number of ways. It might acquire tags that give extra instructions on how to handle it; it might have parts snipped out; it might gain or lose end pieces that make it easier or harder to use. In the normal way of things, the cell employs all of these strategies to control its own functions. In fact, the altering of these RNA messages, so different versions of proteins are made at different times, is key to the process of development. The same gene can be used to make one version of a protein in a human fetus and a different version in an adult.

But as with so many things, once those tools are under the control of an enemy, it’s a different story. A virus that can edit a host’s RNA messages would be able to create versions of proteins that favor a virus’s goals, without ever having to break into the nucleus. And because CMV is known to be somewhat peculiar — it is one of those viruses that don’t suppress hosts’ messages the way many others do — the UCSD group, led by Gene Yeo, a molecular biologist, and Deborah Spector, a virologist, decided to see if it was doing something else to the host’s RNA.

First, the team infected human cells with CMV. Then they extracted the RNA made by the cells at different time points over the course of the infection. The extractions revealed the sum of the chatter between the nucleus and the protein-making machinery. They looked to see how many edits — extra tags, altered end pieces and so on — there were, as compared with healthy, control cells. And while the early stages of infection didn’t show dramatic differences, the late stages, when the infected cells were gearing up to burst and release tons of new viruses, were a different story.

These cells showed more than 2,500 alterations that did not appear in controls, a number that surprised Ron Batra, the UCSD researcher who is first author on the paper and has studied diseases that involve RNA changes. While it isn’t surprising that a virus makes such changes — after all, the goal is to take over the cell, and virologists have known about individual instances of these alterations for some time — the number of edits was striking. That’s as many changes from normal as might be seen in some cancers or ALS, he said. . .

Continue reading.

Things are more complex than one might assume. Evolution has had a lot of time to try variations.

Written by LeisureGuy

6 December 2016 at 3:10 pm

In the Deep, Clues to How Life Makes Light

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Steph Yin reports in Quanta:

Dive deep enough under the surface of the ocean, and light reigns. Some 90 percent of the fish and crustaceans that dwell at depths of 100 to 1,000 meters are capable of making their own light. Flashlight fish hunt and communicate with a flashing Morse code sent by light pockets that pulse under their eyes. Tubeshoulder fish shoot luminous ink at their attackers. Hatchetfish make themselves appear invisible by generating light on their underbellies to mimic downwelling sunlight; predators prowling below look up to see only a continuous glow.

Scientists have indexed thousands of bioluminescent organisms across the tree of life, and they expect to add many more. Yet researchers have long wondered how bioluminescence came to be. Now, as explained in several recently released studies, researchers have made significant progress in understanding the origins of bioluminescence — both evolutionary and chemical. The new understanding may one day allow bioluminescence to be used as a tool in biology and medical research.

One longstanding challenge has been determining how many separate times bioluminescence arose. How many species came to the same conclusion, independent of one another?

Though some of the most familiar examples of light from living organisms are terrestrial — think of fireflies, glowworms and foxfire — the bulk of evolutionary events involving bioluminescence took place in the ocean. Bioluminescence is in fact markedly absent from all terrestrial vertebrates and flowering plants.

In the deep ocean, light gives organisms a unique way to attract prey, communicate and defend themselves, said Matthew Davis, a biologist at St. Cloud State University in Minnesota. In a study released in June, he and his colleagues found that fish that use light for communication and courtship signaling were especially diverse. Over a period of about 150 million years — brief by evolutionary standards —such fish proliferated into more species than other groups of fish. Bioluminescent species that used their light exclusively for camouflage, on the other hand, were no more diverse.

Courtship signals can change relatively easily. These changes can in turn create subgroups in a population, which eventually split into unique species. In June, Todd Oakley, an evolutionary biologist at the University of California, Santa Barbara, and one of his students, Emily Ellis, published a study in which they found that organisms that use bioluminescence in courtship had significantly more species, and faster rates of species accumulation, than closely related organisms that do not use light. Oakley and Ellis studied ten groups of organisms, including fireflies, octopuses, sharks and tiny crustaceans called ostracods.

The study by Davis and his colleagues was limited to ray-finned fishes, a group that includes approximately 95 percent of fish species. Davis estimated that even in that single group, bioluminescence evolved at least 27 times. Steven Haddock, a marine biologist at the Monterey Bay Aquarium Research Institute and an expert on bioluminescence, estimated that across all life forms bioluminescence evolved independently at least 50 times.

Many Ways to Glow

In nearly all shining organisms, bioluminescence requires three ingredients: oxygen, a light-emitting pigment called a luciferin (from the Latin word lucifer, meaning light-bringing), and an enzyme called a luciferase. When a luciferin reacts with oxygen — a process facilitated by luciferase — it forms an excited, unstable compound that emits light when it returns to its lowest energy state.

Curiously, there are far fewer luciferins than luciferases. While species tend to have unique luciferases, many share the same luciferin. Just four luciferins are responsible for most of the light production in the ocean. Of close to 20 groups of bioluminescent organisms in the world, a luciferin called coelenterazine is the light-emitter in nine.

Yet it would be a mistake to assume that all coelenterazine-containing organisms had evolved from a single luminous ancestor. If they had, asked Warren Francis, a biologist at Ludwig Maximilian University in Munich, then why did they develop such a wide variety of luciferases? Presumably the first luciferin-luciferase pair would have survived and multiplied.

It’s more likely that many of these species don’t make coelenterazine themselves. Instead, they get it from their diet, said Yuichi Oba, a professor of biology at Chubu University in Japan.

In 2009, a group led by Oba discovered that the deep-sea copepod — a tiny, near-ubiquitous crustacean — makes its own coelenterazine. These copepods are an extremely abundant food source for a wide range of marine animals — so much so that “in Japan, we call copepods ‘rice in the ocean,’” Oba said. He thinks copepods are key to understanding why so many marine organisms are bioluminescent.

Oba and his colleagues took amino acids believed to be the building blocks of coelenterazine, labeled them with a molecular marker, and loaded them into copepod food. They then fed this food to copepods in the lab.

After 24 hours, the researchers extracted coelenterazine from the copepods and looked for the labels they had added. Sure enough, the labels were there — definitive proof that the crustaceans had synthesized luciferin molecules from the amino acids.

Even the jellyfish in which coelenterazine was first discovered (and named after) was later found not to produce its own coelenterazine at all. It obtains its luciferin by eating copepods and other small crustaceans.

Mysterious Origins

Researchers have found another clue that might help explain the popularity of coelenterazine in deep-sea animals: the molecule also exists in organisms that don’t emit light. This struck Jean-François Rees, a biologist at the Catholic University of Louvain, in Belgium, as odd. It’s already surprising “that so many different animals rely on exactly the same molecule for producing light,” he said. Perhaps coelenterazine had another function besides luminescence?

In experiments with rat liver cells, Rees showed that coelenterazine is a powerful antioxidant.

Many Ways to Glow

In nearly all shining organisms, bioluminescence requires three ingredients: oxygen, a light-emitting pigment called a luciferin (from the Latin word lucifer, meaning light-bringing), and an enzyme called a luciferase. When a luciferin reacts with oxygen — a process facilitated by luciferase — it forms an excited, unstable compound that emits light when it returns to its lowest energy state.

Curiously, there are far fewer luciferins than luciferases. While species tend to have unique luciferases, many share the same luciferin. Just four luciferins are responsible for most of the light production in the ocean. Of close to 20 groups of bioluminescent organisms in the world, a luciferin called coelenterazine is the light-emitter in nine.

Yet it would be a mistake to assume that all coelenterazine-containing organisms had evolved from a single luminous ancestor. If they had, asked Warren Francis, a biologist at Ludwig Maximilian University in Munich, then why did they develop such a wide variety of luciferases? Presumably the first luciferin-luciferase pair would have survived and multiplied.

It’s more likely that many of these species don’t make coelenterazine themselves. Instead, they get it from their diet, said Yuichi Oba, a professor of biology at Chubu University in Japan.

In 2009, a group led by Oba discovered that the deep-sea copepod — a tiny, near-ubiquitous crustacean — makes its own coelenterazine. These copepods are an extremely abundant food source for a wide range of marine animals — so much so that “in Japan, we call copepods ‘rice in the ocean,’” Oba said. He thinks copepods are key to understanding why so many marine organisms are bioluminescent.

Oba and his colleagues took amino acids believed to be the building blocks of coelenterazine, labeled them with a molecular marker, and loaded them into copepod food. They then fed this food to copepods in the lab.

After 24 hours, the researchers extracted coelenterazine from the copepods and looked for the labels they had added. Sure enough, the labels were there — definitive proof that the crustaceans had synthesized luciferin molecules from the amino acids.

Even the jellyfish in which coelenterazine was first discovered (and named after) was later found not to produce its own coelenterazine at all. It obtains its luciferin by eating copepods and other small crustaceans.

Mysterious Origins

Researchers have found another clue that might help explain the popularity of coelenterazine in deep-sea animals: the molecule also exists in organisms that don’t emit light. This struck Jean-François Rees, a biologist at the Catholic University of Louvain, in Belgium, as odd. It’s already surprising “that so many different animals rely on exactly the same molecule for producing light,” he said. Perhaps coelenterazine had another function besides luminescence?

In experiments with rat liver cells, Rees showed that coelenterazine is a powerful antioxidant. . .

Continue reading.

Written by LeisureGuy

1 December 2016 at 10:49 am

Posted in Evolution, Science

Very interesting David Brooks column on whether decision-making is important

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No, hear him out. He has quite a good column in today’s NY Times. I’ll get you started:

Danny Kahneman grew up Jewish in occupied France during World War II. Once in Paris, after curfew, he was nearly captured by an SS officer. His family traveled from town to town through rural France, hiding and hoping people wouldn’t recognize them as Jews. As Michael Lewis writes in his forthcoming book, “The Undoing Project,” Kahneman survived the Holocaust by keeping himself apart.

The family moved to Jerusalem. The army assigned him to a psychological evaluation unit and Kahneman became a psychologist.

Amos Tversky was born in Israel, to a mother who ignored him for long periods so she could serve the nation. He became a paratrooper in the war of 1956, and received one of the nation’s highest awards for bravery after he rescued a man who’d fainted on a torpedo just before it exploded.

Tversky was idiosyncratic. “Amos thought people paid an enormous price to avoid mild embarrassment, and he himself decided early on it was not worth it,” a friend told Lewis.

If he felt like going for a run, he stripped off his pants and went in his underpants. If a social situation bored him, he left. Tversky wasn’t sure how he drifted into psychology. “It’s hard to know how people select a course in life,” he once said. “The big choices we make are practically random.”

Kahneman and Tversky began to work together. They would lock themselves together and talk and laugh, year after year. If they were at a party, they would go off and talk to each other. “When they sat down to write, they nearly merged, physically, into a single form,” Lewis writes, hunched over a single typewriter.

“Their relationship was more intense than a marriage,” Tversky’s wife recalled. When they wrote a paper together they lost all track of who had contributed what. They scrambled for research topics that gave them an excuse to be together, and completed each other’s sentences.

“The way the creative process works is that you first say something and later, sometimes years later, you understand what you said,” Kahneman recalled. “And in our case it was foreshortened. I would say something and Amos understood it. It still gives me goose bumps.”

It was a mystical alchemy that revolutionized how we think about ourselves. Kahneman and Tversky are like a lot of the characters who appear in Michael Lewis’s books, like “Moneyball” and “The Big Short.” They are intellectual renegades who are fervently, almost obsessively, determined to see reality clearly, no matter how ferocious the resistance from everybody else.

While most economics models assumed people were basically rational, Kahneman and Tversky demonstrated that human decision-making is biased in systematic, predictable ways. Many of the biases they described have now become famous — loss aversion, endowment effect, hindsight bias, the anchoring effect, and were described in Kahneman’s brilliant book, “Thinking, Fast and Slow.” They are true giants who have revolutionized how we think about decision-making. Lewis makes academic life seem gripping, which believe it or not, is not easy to do.

My big question is: . . .

Continue reading.

If it’s behind a paywall for you, try googling the first couple of sentences. I think the column is syndicated and you may get a hit for a newspaper that has no paywall.

I included this in the “evolution” category because the systematic biases they discovered have an obvious explanation in evolutionary biology: the biases favor survival, and biases that didn’t were selected against and died out or became rare.

Written by LeisureGuy

25 November 2016 at 10:55 am

Scientists Seek to Update Evolution

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As Creationists like to say, “Evolution is a theory,” and since it is a theory it is constantly open to alteration and adjustment as new evidence is found and new knowledge is gained. (Creationists are not familiar with this device of approaching the truth of reality by successively closer theoretical approximations, though that is how science works, because in their eyes they already have the absolute truth of reality, no changes required, no improvements possible, and if you’re interested, they can explain that to you. Many will have leaflets.)

Carl Zimmer in Quanta discusses a conference on what may be the next paradigm shift in evolution:

Kevin Laland looked out across the meeting room at a couple hundred people gathered for a conference on the future of evolutionary biology. A colleague sidled up next to him and asked how he thought things were going.

“I think it’s going quite well,” Laland said. “It hasn’t gone to fisticuffs yet.”

Laland is an evolutionary biologist who works at the University of St. Andrews in Scotland. On a chilly gray November day, he came down to London to co-host a meeting at the Royal Society called “New Trends in Evolutionary Biology.” A motley crew of biologists, anthropologists, doctors, computer scientists, and self-appointed visionaries packed the room. The Royal Society is housed in a stately building overlooking St. James’s Park. Today the only thing for Laland to see out of the tall meeting-room windows was scaffolding and gauzy tarps set up for renovation work. Inside, Laland hoped, another kind of renovation would be taking place.

In the mid-1900s, biologists updated Darwin’s theory of evolution with new insights from genetics and other fields. The result is often called the Modern Synthesis, and it has guided evolutionary biology for over 50 years. But in that time, scientists have learned a tremendous amount about how life works. They can sequence entire genomes. They can watch genes turn on and off in developing embryos. They can observe how animals and plants respond to changes in the environment.

As a result, Laland and a like-minded group of biologists argue that the Modern Synthesis needs an overhaul. It has to be recast as a new vision of evolution, which they’ve dubbed the Extended Evolutionary Synthesis. Other biologists have pushed back hard, saying there is little evidence that such a paradigm shift is warranted.

This meeting at the Royal Society was the first public conference where Laland and his colleagues could present their vision. But Laland had no interest in merely preaching to the converted, and so he and his fellow organizers also invited prominent evolutionary biologists who are skeptical about the Extended Evolutionary Synthesis.

Both sides offered their arguments and critiques in a civil way, but sometimes you could sense the tension in the room — the punctuations of tsk-tsks, eye-rolling, and partisan bursts of applause.

But no fisticuffs. At least not yet.

Making Evolution as We Know It

Every science passes through times of revolution and of business as usual. After Galileo and Newton dragged physics out of its ancient errors in the 1600s, it rolled forward from one modest advance to the next until the early 1900s. Then Einstein and other scientists established quantum physics, relativity and other new ways of understanding the universe. None of them claimed that Newton was wrong. But it turns out there’s much more to the universe than matter in motion.

Evolutionary biology has had revolutions of its own. The first, of course, was launched by Charles Darwin in 1859 with his book On the Origin of Species.Darwin wove together evidence from paleontology, embryology and other sciences to show that living things were related to one another by common descent. He also introduced a mechanism to drive that long-term change: natural selection. Each generation of a species was full of variations. Some variations helped organisms survive and reproduce, and those were passed down, thanks to heredity, to the next generation.

Darwin inspired biologists all over the world to study animals and plants in a new way, interpreting their biology as adaptations produced over many generations. But he succeeded in this despite having no idea what a gene was. It wasn’t until the 1930s that geneticists and evolutionary biologists came together and recast evolutionary theory. Heredity became the transmission of genes from generation to generation. Variations were due to mutations, which could be shuffled into new combinations. New species arose when populations built up mutations that made interbreeding impossible.

In 1942, the British biologist Julian Huxley described this emerging framework in a book called Evolution: The Modern Synthesis. Today, scientists still call it by that name. (Sometimes they refer to it instead as neo-Darwinism, although that’s actually a confusing misnomer. The term “neo-Darwinism” was actually coined in the late 1800s, to refer to biologists who were advancing Darwin’s ideas in Darwin’s own lifetime.)

The Modern Synthesis proved to be a powerful tool for asking questions about nature. Scientists used it to make a vast range of discoveries about the history of life, such as why some people are prone to genetic disorders like sickle-cell anemia and why pesticides sooner or later fail to keep farm pests in check. But starting not long after the formation of the Modern Synthesis, various biologists would complain from time to time that it was too rigid. It wasn’t until the past few years, however, that Laland and other researchers got organized and made a concerted effort to formulate an extended synthesis that might take its place.

The researchers don’t argue that the Modern Synthesis is wrong — just that it doesn’t capture the full richness of evolution. Organisms inherit more than just genes, for example: They can inherit other cellular molecules, as well as behaviors they learn and the environments altered by their ancestors. Laland and his colleagues also challenge the pre-eminent place that natural selection gets in explanations for how life got to be the way it is. Other processes can influence the course of evolution, too, from the rules of development to the environments in which organisms have to live.

“It’s not simply bolting more mechanisms on what we already have,” said Laland. “It requires you to think of causation in a different way.”

Adding to Darwin

Eva Jablonka, a biologist at Tel Aviv University, used her talk to explore the evidence for a form of heredity beyond genes. . .

Continue reading.

Written by LeisureGuy

22 November 2016 at 2:50 pm

Posted in Evolution, Science

A Conductor of Evolution’s Subtle Symphony

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I am still amazed that people believe that they can “deny” the reality of evolution—it’s as though they deny the reality of the sun. The fact is that the evidence for evolution is overwhelming, plus it makes perfect sense in terms of general principles (in any environment, some variations will fare better than others). Stephanie Bucklin interviews Richard Lenski in Quanta:

Early in his career, the decorated biologist Richard Lenski thought he might be forced to evolve. After his postdoctoral research grant was canceled, Lenski began to look tentatively at other options. With one child and a second on the way, Lenski attended a seminar about using specific types of data in an actuarial context — the same type of data he had worked with as a graduate student. Lenski collected a business card from the speaker, thinking he might be able to make use of his background in a new career.

“But then, as it sometimes does — and I was very lucky — the tide turned,” Lenski told Quanta Magazine in his high-rise office at Michigan State University. “We got the grant renewed, and soon thereafter, I started getting faculty offers.”

Lenski, a professor of microbial ecology at Michigan State, is best known for his work on what’s known as the long-term evolution experiment. The project, started in 1988, examines evolution in action. He and his lab members have been growing 12 populations of E. coli continuously for over 65,000 generations, tracking the development and mutations of the 12 separate strains.

The results have garnered attention and accolades — including a MacArthur “genius” grant, which Lenski received in 1996 — both for the enormity of the undertaking and for the intriguing findings the study has yielded. Most notably, in 2003, Lenski and his collaborators realized that one strain of E. coli had evolved the ability to use citrate as an energy source, something no previous population of E. coli was able to do.

Lenski is also interested in digital organisms, computer programs that have been designed to mimic the process of evolution. He was instrumental in the push to open the Beacon Center at Michigan State, which gives computer scientists and evolutionary biologists the opportunity to forge unique collaborations.

Quanta Magazine met with Lenski in his office to talk about his own evolving interests in the field of evolutionary biology — and about the time he almost pulled the plug on the long-term experiment. An edited and condensed version of the conversation follows.

QUANTA MAGAZINE: What sort of questions have been driving forces in your career?

RICHARD LENSKI: One question that has always intrigued me is about the reproducibility or repeatability of evolution. Stephen Jay Gould, the paleontologist and historian of science, posed this question: If we could rewind the tape of life on Earth, how similar or dissimilar would it be if we watched the whole process play out again? The long-term experiment that we do has allowed us to gather a lot of data about this question.

So is evolution repeatable?

Yes and no! I sometimes tell people it’s been a fascinating motivating question, but on one level, it is a terrible question, and one you would never tell a graduate student to go after. That’s because it is very open-ended, and it does not have a very clear-cut answer.

From the long-term experiment, we’ve seen some really beautiful examples of things that are remarkably reproducible, and on the other hand some other crazy things where one population goes off and does things that are entirely different from the other 11 populations in the experiment.

How did you first come up with the idea for the long-term experiment?

I had been working already for several years on experimental evolution with bacteria, as well as viruses that infect bacteria. Those were fascinating, but everything became so complicated so quickly that I said, “Let’s reduce evolution down to its bare bones.” In particular, I wanted to go after this question of reproducibility or repeatability of evolution. And if I wanted to be able to look at the reproducibility of evolution, I wanted a system that was very simple. When I started the long-term experiment, my original goal was that I would call it the long-term experiment when I got to 2,000 generations.

How long did that take you?

The actual running of the experiment was about 10 or 11 months, but by the time we had collected data, wrote it up, and got the paper published, it was more like two and a half years or so. By then the experiment had already passed 5,000 generations, and I realized we should keep it going.

Did you anticipate the experiment going on for as long as it has?

No. No, I didn’t. There was a five-year period, maybe from the late ’90s into the early 2000s, where I thought about possibly stopping the experiment. This was for a couple of different reasons. One was that I was getting hooked on this other way of studying evolution, which involved looking at evolution in self-replicating computer programs, which was absolutely fascinating. Suddenly I saw this even shinier way of studying evolution, where it could go even more generations and do even more, seemingly neater, experiments.

How have your views on studying evolution via these digital organisms changed over time?

I had this sort of “puppy love” when I first learned about it. At first, it was just so extraordinarily interesting and exciting to be able to watch self-replicating programs, to be able to change their environments, and to watch evolution happen.

One of the really exciting things about digital evolution is that it shows that we think of evolution as being about stuff with blood and guts and DNA and RNA and proteins. But the idea of evolution really comes down to some very basic ideas of heredity, replication and competition. The philosopher of science Daniel Dennett has emphasized that we see evolution as this instantiation, this form of biological life, but the principals of it are much more general than that.

I would say that my latest directions of research have been primarily by way of talking with super-smart colleagues and serving on committees of graduate students who are using these systems. I’m less involved in designing experiments or formulating specific hypotheses, because that field has been moving extremely quickly. I feel I was very lucky to pick off some of the low-hanging fruit, but now I feel like I’m in there as a biologist, maybe criticizing hypotheses, suggesting controls that might be done in some experiments.

So your interest in digital organisms was one reason you considered shutting down the long-term experiment. What was the other? . . .

Continue reading.

Written by LeisureGuy

8 November 2016 at 12:41 pm

Posted in Evolution, Science

In Newly Created Life-Form, a Major Mystery

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Emily Singer reports in Quanta:

Peel away the layers of a house — the plastered walls, the slate roof, the hardwood floors — and you’re left with a frame, the skeletal form that makes up the core of any structure. Can we do the same with life? Can scientists pare down the layers of complexity to reveal the essence of life, the foundation on which biology is built?

That’s what Craig Venter and his collaborators have attempted to do in a new study published today in the journal Science. Venter’s team painstakingly whittled down the genome ofMycoplasma mycoides, a bacterium that lives in cattle, to reveal a bare-bones set of genetic instructions capable of making life. The result is a tiny organism named syn3.0 that contains just 473 genes. (By comparison, E. colihas about 4,000 to 5,000 genes, and humans have roughly 20,000.)

Yet within those 473 genes lies a gaping hole. Scientists have little idea what roughly a third of them do. Rather than illuminating the essential components of life, syn3.0 has revealed how much we have left to learn about the very basics of biology.

“To me, the most interesting thing is what it tells us about what we don’t know,” said Jack Szostak, a biochemist at Harvard University who was not involved in the study. “So many genes of unknown function seem to be essential.”

“We were totally surprised and shocked,” said Venter, a biologist who heads the J. Craig Venter Institute in La Jolla, Calif., and Rockville, Md., and is most famous for his role in mapping the human genome. The researchers had expected some number of unknown genes in the mix, perhaps totaling five to 10 percent of the genome. “But this is truly a stunning number,” he said.

The seed for Venter’s quest was planted in 1995, when his team deciphered the genome of Mycoplasma genitalium, a microbe that lives in the human urinary tract. When Venter’s researchers started work on this new project, they chose M. genitalium — the second complete bacterial genome to be sequenced — expressly for its diminutive genome size. With 517 genes and 580,000 DNA letters, it has one of the smallest known genomes in a self-replicating organism. (Some symbiotic microbes can survive with just 100-odd genes, but they rely on resources from their host to survive.)

M. genitalium’s trim package of DNA raised the question: What is the smallest number of genes a cell could possess? “We wanted to know the basic gene components of life,” Venter said. “It seemed like a great idea 20 years ago — we had no idea it would be a 20-year process to get here.”

Minimal Design

Venter and his collaborators originally set out to design a stripped-down genome based on what scientists knew about biology. They would start with genes involved in the most critical processes of the cell, such as copying and translating DNA, and build from there.

But before they could create this streamlined version of life, the researchers had to figure out how to design and build genomes from scratch. Rather than editing DNA in a living organism, as most researchers did, they wanted to exert greater control — to plan their genome on a computer and then synthesize the DNA in test tubes.

In 2008, Venter and his collaborator Hamilton Smith created the first synthetic bacterial genome by building a modified version of M. genitalium’s DNA. Then in 2010 they made the first self-replicating synthetic organism, manufacturing a version of M. mycoides’ genome and then transplanting it into a different Mycoplasma species. The synthetic genome took over the cell, replacing the native operating system with a human-made version. The synthetic M. mycoides genome was mostly identical to the natural version, save for a few genetic watermarks — researchers added their names and a few famous quotes, including a slightly garbled version of Richard Feynman’s assertion, “What I cannot create, I do not understand.”

With the right tools finally in hand, the researchers designed a set of genetic blueprints for their minimal cell and then tried to build them. Yet “not one design worked,” Venter said. He saw their repeated failures as a rebuke for their hubris. Does modern science have sufficient knowledge of basic biological principles to build a cell? “The answer was a resounding no,” he said.

So the team took a different and more labor-intensive tack, replacing the design approach with trial and error. They disrupted M. mycoides’ genes, determining which were essential for the bacteria to survive. They erased the extraneous genes to create syn3.0, which has a smaller genome than any independently replicating organism discovered on Earth to date.

What’s left after trimming the genetic fat? . . .

Continue reading.

Written by LeisureGuy

27 October 2016 at 12:28 pm

Posted in Evolution, Science

Fascinating: Why snakes now have no legs. (They once did.)

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First, watch this brief (less then 3 minutes) video; then read this article by Madison Margolin in Motherboard.

Written by LeisureGuy

26 October 2016 at 12:24 pm

Posted in Evolution, Science, Video

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