A Momentary Flow

Updating Worldviews one World at a time

Neuroscientists identify key role of language gene
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Neuroscientists have found that a gene mutation that arose more than half a million years ago may be key to humans’ unique ability to produce and understand speech. Researchers from MIT and several European universities have shown that the human version of a gene called Foxp2 makes it easier to transform new experiences into routine procedures. When they engineered mice to express humanized Foxp2, the mice learned to run a maze much more quickly than normal mice. The findings suggest that Foxp2 may help humans with a key component of learning language — transforming experiences, such as hearing the word “glass” when we are shown a glass of water, into a nearly automatic association of that word with objects that look and function like glasses, says Ann Graybiel, an MIT Institute Professor, member of MIT’s McGovern Institute for Brain Research, and a senior author of the study. “This really is an important brick in the wall saying that the form of the gene that allowed us to speak may have something to do with a special kind of learning, which takes us from having to make conscious associations in order to act to a nearly automatic-pilot way of acting based on the cues around us,” Graybiel says. Wolfgang Enard, a professor of anthropology and human genetics at Ludwig-Maximilians University in Germany, is also a senior author of the study, which appears in the Proceedings of the National Academy of Sciences this week. The paper’s lead authors are Christiane Schreiweis, a former visiting graduate student at MIT, and Ulrich Bornschein of the Max Planck Institute for Evolutionary Anthropology in Germany. All animal species communicate with each other, but humans have a unique ability to generate and comprehend language. Foxp2 is one of several genes that scientists believe may have contributed to the development of these linguistic skills. The gene was first identified in a group of family members who had severe difficulties in speaking and understanding speech, and who were found to carry a mutated version of the Foxp2 gene. In 2009, Svante Pääbo, director of the Max Planck Institute for Evolutionary Anthropology, and his team engineered mice to express the human form of the Foxp2 gene, which encodes a protein that differs from the mouse version by only two amino acids. His team found that these mice had longer dendrites — the slender extensions that neurons use to communicate with each other — in the striatum, a part of the brain implicated in habit formation. They were also better at forming new synapses, or connections between neurons. (via Neuroscientists identify key role of language gene — ScienceDaily)

Neuroscientists identify key role of language gene
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Neuroscientists have found that a gene mutation that arose more than half a million years ago may be key to humans’ unique ability to produce and understand speech. Researchers from MIT and several European universities have shown that the human version of a gene called Foxp2 makes it easier to transform new experiences into routine procedures. When they engineered mice to express humanized Foxp2, the mice learned to run a maze much more quickly than normal mice. The findings suggest that Foxp2 may help humans with a key component of learning language — transforming experiences, such as hearing the word “glass” when we are shown a glass of water, into a nearly automatic association of that word with objects that look and function like glasses, says Ann Graybiel, an MIT Institute Professor, member of MIT’s McGovern Institute for Brain Research, and a senior author of the study. “This really is an important brick in the wall saying that the form of the gene that allowed us to speak may have something to do with a special kind of learning, which takes us from having to make conscious associations in order to act to a nearly automatic-pilot way of acting based on the cues around us,” Graybiel says. Wolfgang Enard, a professor of anthropology and human genetics at Ludwig-Maximilians University in Germany, is also a senior author of the study, which appears in the Proceedings of the National Academy of Sciences this week. The paper’s lead authors are Christiane Schreiweis, a former visiting graduate student at MIT, and Ulrich Bornschein of the Max Planck Institute for Evolutionary Anthropology in Germany. All animal species communicate with each other, but humans have a unique ability to generate and comprehend language. Foxp2 is one of several genes that scientists believe may have contributed to the development of these linguistic skills. The gene was first identified in a group of family members who had severe difficulties in speaking and understanding speech, and who were found to carry a mutated version of the Foxp2 gene. In 2009, Svante Pääbo, director of the Max Planck Institute for Evolutionary Anthropology, and his team engineered mice to express the human form of the Foxp2 gene, which encodes a protein that differs from the mouse version by only two amino acids. His team found that these mice had longer dendrites — the slender extensions that neurons use to communicate with each other — in the striatum, a part of the brain implicated in habit formation. They were also better at forming new synapses, or connections between neurons. (via Neuroscientists identify key role of language gene — ScienceDaily)

Evolution’s Random Paths Lead to One Place - A massive statistical study suggests that the final evolutionary outcome — fitness — is predictable. - In his fourth-floor lab at Harvard University, Michael Desai has created hundreds of identical worlds in order to watch evolution at work. Each of his meticulously controlled environments is home to a separate strain of baker’s yeast. Every 12 hours, Desai’s robot assistants pluck out the fastest-growing yeast in each world — selecting the fittest to live on — and discard the rest. Desai then monitors the strains as they evolve over the course of 500 generations. His experiment, which other scientists say is unprecedented in scale, seeks to gain insight into a question that has long bedeviled biologists: If we could start the world over again, would life evolve the same way? Many biologists argue that it would not, that chance mutations early in the evolutionary journey of a species will profoundly influence its fate. “If you replay the tape of life, you might have one initial mutation that takes you in a totally different direction,” Desai said, paraphrasing an idea first put forth by the biologist Stephen Jay Gould in the 1980s. Desai’s yeast cells call this belief into question. According to results published in Science in June, all of Desai’s yeast varieties arrived at roughly the same evolutionary endpoint (as measured by their ability to grow under specific lab conditions) regardless of which precise genetic path each strain took. It’s as if 100 New York City taxis agreed to take separate highways in a race to the Pacific Ocean, and 50 hours later they all converged at the Santa Monica pier. The findings also suggest a disconnect between evolution at the genetic level and at the level of the whole organism. Genetic mutations occur mostly at random, yet the sum of these aimless changes somehow creates a predictable pattern. The distinction could prove valuable, as much genetics research has focused on the impact of mutations in individual genes. For example, researchers often ask how a single mutation might affect a microbe’s tolerance for toxins, or a human’s risk for a disease. But if Desai’s findings hold true in other organisms, they could suggest that it’s equally important to examine how large numbers of individual genetic changes work in concert over time. “There’s a kind of tension in evolutionary biology between thinking about individual genes and the potential for evolution to change the whole organism,” said Michael Travisano, a biologist at the University of Minnesota. “All of biology has been focused on the importance of individual genes for the last 30 years, but the big take-home message of this study is that’s not necessarily important.” (via Yeast Study Suggests Genetics Are Random but Evolution Is Not | Simons Foundation)

Evolution’s Random Paths Lead to One Place
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A massive statistical study suggests that the final evolutionary outcome — fitness — is predictable.
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In his fourth-floor lab at Harvard University, Michael Desai has created hundreds of identical worlds in order to watch evolution at work. Each of his meticulously controlled environments is home to a separate strain of baker’s yeast. Every 12 hours, Desai’s robot assistants pluck out the fastest-growing yeast in each world — selecting the fittest to live on — and discard the rest. Desai then monitors the strains as they evolve over the course of 500 generations. His experiment, which other scientists say is unprecedented in scale, seeks to gain insight into a question that has long bedeviled biologists: If we could start the world over again, would life evolve the same way? Many biologists argue that it would not, that chance mutations early in the evolutionary journey of a species will profoundly influence its fate. “If you replay the tape of life, you might have one initial mutation that takes you in a totally different direction,” Desai said, paraphrasing an idea first put forth by the biologist Stephen Jay Gould in the 1980s. Desai’s yeast cells call this belief into question. According to results published in Science in June, all of Desai’s yeast varieties arrived at roughly the same evolutionary endpoint (as measured by their ability to grow under specific lab conditions) regardless of which precise genetic path each strain took. It’s as if 100 New York City taxis agreed to take separate highways in a race to the Pacific Ocean, and 50 hours later they all converged at the Santa Monica pier. The findings also suggest a disconnect between evolution at the genetic level and at the level of the whole organism. Genetic mutations occur mostly at random, yet the sum of these aimless changes somehow creates a predictable pattern. The distinction could prove valuable, as much genetics research has focused on the impact of mutations in individual genes. For example, researchers often ask how a single mutation might affect a microbe’s tolerance for toxins, or a human’s risk for a disease. But if Desai’s findings hold true in other organisms, they could suggest that it’s equally important to examine how large numbers of individual genetic changes work in concert over time. “There’s a kind of tension in evolutionary biology between thinking about individual genes and the potential for evolution to change the whole organism,” said Michael Travisano, a biologist at the University of Minnesota. “All of biology has been focused on the importance of individual genes for the last 30 years, but the big take-home message of this study is that’s not necessarily important.” (via Yeast Study Suggests Genetics Are Random but Evolution Is Not | Simons Foundation)

'Smart genes' prove elusive - Study of more than 100,000 people finds three genetic variants for IQ — but their effects are maddeningly small. - Scientists looking for the genes underlying intelligence are in for a slog. One of the largest, most rigorous genetic studies of human cognition1 has turned up inconclusive findings, and experts concede that they will probably need to scour the genomes of more than 1 million people to confidently identify even a small genetic influence on intelligence and other behavioural traits.Studies of twins have repeatedly confirmed a genetic basis for intelligence, personality and other aspects of behaviour. But efforts to link IQ to specific variations in DNA have led to a slew of irreproducible results. Critics have alleged that some of these studies’ methods were marred by wishful thinking and shoddy statistics. A sobering editorial in the January 2012 issue of Behavior Genetics2 declared that “it now seems likely that many of the published findings of the last decade are wrong or misleading and have not contributed to real advances in knowledge”. (via 'Smart genes' prove elusive : Nature News & Comment)

'Smart genes' prove elusive
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Study of more than 100,000 people finds three genetic variants for IQ — but their effects are maddeningly small.
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Scientists looking for the genes underlying intelligence are in for a slog. One of the largest, most rigorous genetic studies of human cognition1 has turned up inconclusive findings, and experts concede that they will probably need to scour the genomes of more than 1 million people to confidently identify even a small genetic influence on intelligence and other behavioural traits.Studies of twins have repeatedly confirmed a genetic basis for intelligence, personality and other aspects of behaviour. But efforts to link IQ to specific variations in DNA have led to a slew of irreproducible results. Critics have alleged that some of these studies’ methods were marred by wishful thinking and shoddy statistics. A sobering editorial in the January 2012 issue of Behavior Genetics2 declared that “it now seems likely that many of the published findings of the last decade are wrong or misleading and have not contributed to real advances in knowledge”. (via 'Smart genes' prove elusive : Nature News & Comment)

Yet viewing our genome as an elegant and tidy blueprint for building humans misses a crucial fact: our genome does not exist to serve us humans at all. Instead, we exist to serve our genome, a collection of genes that have been surviving from time immemorial, skipping down the generations. These genes have evolved to build human ‘survival machines’, programmed as tools to make additional copies of the genes (by producing more humans who carry them in their genomes). From the cold-hearted view of biological reality, we exist only to ensure the survival of these travellers in our genomes.

Is our genome full of junk DNA? – Itai Yanai and Martin Lercher – Aeon
Life doesn’t make trash - A genome is not a blueprint for building a human being, so is there any way to judge whether DNA is junk or not? - Humans are astounding creatures, our unique and highly complex traits encoded by our genome – a vast sequence of DNA ‘letters’ (called nucleotides) directing the building and maintenance of the body and brain. Yet science has served up the confounding paradox that the bulk of our genome appears to be dead wood, biologically inert junk. Could all this mysterious ‘dark matter’ in our genome really be non-functional? Our genome has more than 20,000 genes, relatively stable stretches of DNA transmitted largely unchanged between generations. These genes contain recipes for molecules, especially proteins, that are the main building blocks and molecular machines of our bodies. Yet DNA that codes for such known structures accounts for just over 3 per cent of our genome. What about the other 97 per cent? With the publication of the first draft of the human genome in 2001, that shadow world came into focus. It emerged that roughly half our DNA consisted of ‘repeats’, long stretches of letters sometimes found in millions of copies at seemingly random places throughout the genome. Were all these repeats just junk? To answer this question, hundreds of scientists worldwide joined a massive science project called the Encyclopedia of DNA Elements, or ENCODE. After working hard for almost a decade, in 2012 ENCODE came to a surprising conclusion: rather than being composed mostly of useless junk, 80 per cent of the human genome is in fact functional. (via Is our genome full of junk DNA? – Itai Yanai and Martin Lercher – Aeon)

Life doesn’t make trash
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A genome is not a blueprint for building a human being, so is there any way to judge whether DNA is junk or not?
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Humans are astounding creatures, our unique and highly complex traits encoded by our genome – a vast sequence of DNA ‘letters’ (called nucleotides) directing the building and maintenance of the body and brain. Yet science has served up the confounding paradox that the bulk of our genome appears to be dead wood, biologically inert junk. Could all this mysterious ‘dark matter’ in our genome really be non-functional? Our genome has more than 20,000 genes, relatively stable stretches of DNA transmitted largely unchanged between generations. These genes contain recipes for molecules, especially proteins, that are the main building blocks and molecular machines of our bodies. Yet DNA that codes for such known structures accounts for just over 3 per cent of our genome. What about the other 97 per cent? With the publication of the first draft of the human genome in 2001, that shadow world came into focus. It emerged that roughly half our DNA consisted of ‘repeats’, long stretches of letters sometimes found in millions of copies at seemingly random places throughout the genome. Were all these repeats just junk? To answer this question, hundreds of scientists worldwide joined a massive science project called the Encyclopedia of DNA Elements, or ENCODE. After working hard for almost a decade, in 2012 ENCODE came to a surprising conclusion: rather than being composed mostly of useless junk, 80 per cent of the human genome is in fact functional. (via Is our genome full of junk DNA? – Itai Yanai and Martin Lercher – Aeon)

I Contain Multitudes /Our bodies are a genetic patchwork, possessing variation from cell to cell. Is that a good thing? / Your DNA is supposed to be your blueprint, your unique master code, identical in every one of your tens of trillions of cells. It is why you are you, indivisible and whole, consistent from tip to toe. But that’s really just a biological fairy tale. In reality, you are an assemblage of genetically distinctive cells, some of which have radically different operating instructions. This fact has only become clear in the last decade. Even though each of your cells supposedly contains a replica of the DNA in the fertilized egg that began your life, mutations, copying errors and editing mistakes began modifying that code as soon as your zygote self began to divide. In your adult body, your DNA is peppered by pinpoint mutations, riddled with repeated or rearranged or missing information, even lacking huge chromosome-sized chunks. Your data is hopelessly corrupt. Most genome scientists assume that this DNA diversity, called “somatic mutation” or “structural variation,” is bad. Mutations and other genetic changes can alter the function of the cell, usually for the worse. Disorderly DNA is a hallmark of cancers, and genomic variation can cause a suite of brain disorders and malformations. It makes sense: Cells working off garbled information probably don’t function very well. Most research to date has focused on how aberrant DNA drives disease, but even healthy bodies harbor genetic disorder. In the last few years, some researchers report that anywhere from 10 to 40 percent of brain cells and between 30 and 90 percent of human liver cells are aneuploid, meaning that one entire chromosome is either missing or duplicated. Copy number variations, in which chunks of DNA between 100 and a few million letters in length are multiplied or eliminated, also seem to be widespread in healthy people. (via Our Body as Genetic Patchwork: Helpful or Hurtful? | Simons Foundation)

I Contain Multitudes
/
Our bodies are a genetic patchwork, possessing variation from cell to cell. Is that a good thing?
/
Your DNA is supposed to be your blueprint, your unique master code, identical in every one of your tens of trillions of cells. It is why you are you, indivisible and whole, consistent from tip to toe. But that’s really just a biological fairy tale. In reality, you are an assemblage of genetically distinctive cells, some of which have radically different operating instructions. This fact has only become clear in the last decade. Even though each of your cells supposedly contains a replica of the DNA in the fertilized egg that began your life, mutations, copying errors and editing mistakes began modifying that code as soon as your zygote self began to divide. In your adult body, your DNA is peppered by pinpoint mutations, riddled with repeated or rearranged or missing information, even lacking huge chromosome-sized chunks. Your data is hopelessly corrupt. Most genome scientists assume that this DNA diversity, called “somatic mutation” or “structural variation,” is bad. Mutations and other genetic changes can alter the function of the cell, usually for the worse. Disorderly DNA is a hallmark of cancers, and genomic variation can cause a suite of brain disorders and malformations. It makes sense: Cells working off garbled information probably don’t function very well. Most research to date has focused on how aberrant DNA drives disease, but even healthy bodies harbor genetic disorder. In the last few years, some researchers report that anywhere from 10 to 40 percent of brain cells and between 30 and 90 percent of human liver cells are aneuploid, meaning that one entire chromosome is either missing or duplicated. Copy number variations, in which chunks of DNA between 100 and a few million letters in length are multiplied or eliminated, also seem to be widespread in healthy people. (via Our Body as Genetic Patchwork: Helpful or Hurtful? | Simons Foundation)

Evolution and Entropy
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One of the surprising discoveries of Papadimitriou’s study is that natural selection values not just fitness, but also genetic diversity, which in more technical terms is referred to as entropy. This view that evolution optimizes not just mean fitness but mean fitness and entropy is not well known, “but I think it’s a deep observation,” Adami said. The Berkeley team isn’t the first to highlight the role entropy might play in evolution. But until now, the subject has mainly been of interest to mathematicians rather than biologists. “Applications of entropy in evolution have had a bad name, because they were very ill-defined,” Barton said. “More recently, there have been some interesting, and much sounder, ideas, which make a link between fields that are addressing a similar issue: Statistical physics and evolutionary biology both try to understand the overall properties of a complicated system, independent of the microscopic details.” These more recent results are mathematically sound, but they still don’t connect well with existing biological understanding, he said. “So it’s not clear to biologists how [the results] might help explain their open questions.”

Game Theory Makes New Predictions for Evolution | Simons Foundation
The Game Theory of Life
-Applying game theory to the behavior of genes provides a new view of natural selection. - In what appears to be the first study of its kind, computer scientists report that an algorithm discovered more than 50 years ago in game theory and now widely used in machine learning is mathematically identical to the equations used to describe the distribution of genes within a population of organisms. Researchers may be able to use the algorithm, which is surprisingly simple and powerful, to better understand how natural selection works and how populations maintain their genetic diversity. By viewing evolution as a repeated game, in which individual players, in this case genes, try to find a strategy that creates the fittest population, researchers found that evolution values both diversity and fitness. Some biologists say that the findings are too new and theoretical to be of use; researchers don’t yet know how to test the ideas in living organisms. Others say the surprising connection, published Monday in the advance online version of the Proceedings of the National Academy of Sciences, may help scientists understand a puzzling feature of natural selection: The fittest organisms don’t always wipe out their weaker competition. Indeed, as evidenced by the menagerie of life on Earth, genetic diversity reigns. “It’s a very different way to look at selection,” said Stephen Stearns, an evolutionary biologist at Yale University who was not involved in the study. “I always find radically different ways of looking at a problem interesting.” (via Game Theory Makes New Predictions for Evolution | Simons Foundation)

The Game Theory of Life

-Applying game theory to the behavior of genes provides a new view of natural selection.
-
In what appears to be the first study of its kind, computer scientists report that an algorithm discovered more than 50 years ago in game theory and now widely used in machine learning is mathematically identical to the equations used to describe the distribution of genes within a population of organisms. Researchers may be able to use the algorithm, which is surprisingly simple and powerful, to better understand how natural selection works and how populations maintain their genetic diversity. By viewing evolution as a repeated game, in which individual players, in this case genes, try to find a strategy that creates the fittest population, researchers found that evolution values both diversity and fitness. Some biologists say that the findings are too new and theoretical to be of use; researchers don’t yet know how to test the ideas in living organisms. Others say the surprising connection, published Monday in the advance online version of the Proceedings of the National Academy of Sciences, may help scientists understand a puzzling feature of natural selection: The fittest organisms don’t always wipe out their weaker competition. Indeed, as evidenced by the menagerie of life on Earth, genetic diversity reigns.
“It’s a very different way to look at selection,” said Stephen Stearns, an evolutionary biologist at Yale University who was not involved in the study. “I always find radically different ways of looking at a problem interesting.” (via Game Theory Makes New Predictions for Evolution | Simons Foundation)