The Theory of Bilateral Subjective Adaptation
The Elements of the Theory
Natural Selection Is a Proven Theory or It's Not
Natural selection clearly exists. Random positive mutations over long periods of time allow creatures better reproductive success. There is clear evidence of slow adaptive change in form in particular creatures. But there is very limited evidence that that creates new species. Stephen Jay Gould's theory of punctuated equilibrium is one answer proposed to explain this. I have a theory that proposes something radically different. It proposes that genetic change can be very fast and clearly not a random process of change in the genome that allows adaptive advantage. What follows is a short description of my new theory and supporting studies that show that genetic change can be very fast and clearly not a random process, something I call genomic plasticity. Like all science and every accepted theory, the theory must explain even the exceptions. Because Darwin's theory of natural selection came with what was felt to be overwhelming evidence, it is said to be a proven theory that explains how life works. In the same way, Newtonian mechanics was once thought to explain nature in a complete way until Einstein came along and showed that some of its assumptions were inadequate. The foundation of Newtonian mechanics describing space and time, action and reaction was changed with Einstein's theory of relativity. And even Einstein thought with that addition, there was a complete description of natural process. Quantum mechanics proved that wasn't true. Einstein himself never really accepted the fundamental premises of quantum mechanics that upended the idea of cause and effect and predictable outcomes. My theory of bilateral subjective adaptation is as fundamentally different to natural selection as Newtonian mechanics is to quantum mechanics. My theory is based on the idea that nature expresses bilateral forms at every level; matter/antimatter, entropy/complexity, and every level of life expresses the Nash equilibrium that says the division of limited resources is best accomplished when creatures act in their own self-interest AND the interest of the group to which they belong. My theory proposes that because complexity is a fundamental aspect of nature, evolution is not completely undirected. It has a purpose, and that purpose is to develop expressions of subjective complexity. Because subjective awareness is necessary if creatures are to act in the shared interest of the group to which they belong, then subjective awareness must become more complex as ecosystems become more complex. With every one of the nine steps of subjective complexity, ecosystems geometrically exploded with new possibilities and new species. With new senses and more complex brains to process information about the environment and the ecosystem that included so many other species, countless new forms had new meaning and purpose responding to such new subjective complexity. Natural selection does exist just like Newtonian mechanics exists, but bilateral subjective adaptation exists as well directed by the subjective awareness necessary for all creatures in the ecosystems to which they belong. Breeding Arctic foxes for shorter flight distances not only changed the shape and colour and skulls of offspring and turned them from vicious fighters to docile creatures that would answer to their given names, but that fundamental change happened in just a few generations. In effect changing one subjective response created a new species of fox completely unlike its ancestor in form and behaviour. I propose that particular species and sometimes particular individuals have a genomic plasticity that allows the creation of new species and short periods of time. That genomic plasticity allows the genome to express traits from places in the genome that are no longer expressed in that individual or species. We share far more traits with orangutans than we do with bonobos even though we last shared a common ancestor with orangutans 17 million years ago, many millions of years before the common ancestor we share with chimpanzees. I believe that the studies I cite offer overwhelming evidence that bilateral subjective adaptation and genomic plasticity not only exists, but it is in fact the primary origin of new species. I do not expect my theory to be accepted by any but a few open minded individuals. It took 50 years before natural selection was accepted science. So like every good scientific theory, it must stand the test of time and critical review. So, remember what the dormouse said.... Best Evidence
Mark Stoeckle from The Rockefeller University in New York and David Thaler at the University of Basel in Switzerland, who together published findings last week sure to jostle, if not overturn, more than one settled idea about how evolution unfolds. It is textbook biology, for example, that species with large, far-flung populations—think ants, rats, humans—will become more genetically diverse over time. But is that true? “The answer is no,” said Stoeckle, lead author of the study, published in the journal Human Evolution. For the planet’s 7.6 billion people, 500 million house sparrows, or 100,000 sandpipers, genetic diversity “is about the same,” he told AFP. The study’s most startling result, perhaps, is that nine out of 10 species on Earth today, including humans, came into being 100,000 to 200,000 years ago. “This conclusion is very surprising, and I fought against it as hard as I could,” Thaler told AFP. That reaction is understandable: How does one explain the fact that 90 percent of animal life, genetically speaking, is roughly the same age? Well, what about mutation and selection? Couldn’t they create all this information in a couple hundred thousand years? Well, no. You see, mutation and selection have been tested in the lab to see how much information they can produce over generations and generations. And the conclusion is clear: it is impossible for blind forces to create the amount of information we see in living systems in the short time that is available. In fact, the whole history of the universe is not enough time for evolutionary mechanisms to create the information we have in front of us. Before we leave the paper reported by Phys.org, here is something about whether we see the gradual emergence of complexity via lots of transitional forms in nature. Not so much: […][A]nother unexpected finding from the study—species have very clear genetic boundaries, and there’s nothing much in between. “If individuals are stars, then species are galaxies,” said Thaler. “They are compact clusters in the vastness of empty sequence space.” The absence of “in-between” species is something that also perplexed Darwin, he said. Indeed. So perplexing. Proof of the Nash Equilibrium
More than 50 years ago on the shoreline of a rocky tide pool, the US ecologist Robert Paine found out that the removal of a single species from an ecosystem could dramatically alter its structure and function. He had discovered that starfish act as a keystone species in that their presence and role as a top predator maintained the coexistence of diverse species in the rocky intertidal zone. Plant defense genes tested with a simplified ecosystem in the lab A team of ecologists and geneticists at the University of Zurich (UZH) and the University of California, Davis have now found that a mutation at a single gene can also dramatically alter the structure and function of an ecosystem. The study, published in Science, suggests that a gene not only encodes information that determines an organism's fitness, but can also influence the persistence of interacting species in an ecological community. The discovery of Jordi Bascompte, professor at the UZH Department of Evolutionary Biology and Environmental Studies, and his team was made using an experimental ecosystem in the lab with a predator (a parasitic wasp), two herbivores (aphids), and the plant Arabidopsis thaliana -- a genetic model organism. "Keystone gene" can prevent ecosystem from collapsing The researchers tested the effect of three plant genes that control the plant's natural arsenal of chemical defenses against herbivores. They found that the herbivores and predator in their experimental community were more likely to survive on plants with a mutation at a single gene called AOP2. "This natural mutation at AOP2 not only affected the plant's chemistry, but also made the plant grow faster, which in turn helped the herbivores and predator coexist, thereby preventing the ecosystem from collapsing," UZH scientist and first author Matt Barbour explains. Similar to a keystone species such as the starfish, AOP2 acts as a "keystone gene" that is critical to the survival of the experimental ecosystem. Impacts on current biodiversity conservation The discovery of a keystone gene is likely to have implications on how to conserve biodiversity in a changing world. In particular, knowledge from genetics and ecological networks should be included when it comes to predicting the consequences of genetic change for the persistence of biodiversity across scales. Individuals with different variants of a gene or even genetically modified organisms could be added to existing populations to foster more diverse and resilient ecosystems. However, a seemingly small genetic change could unleash a cascade of unintended consequences for ecosystems if not studied in detail first. "We're only just beginning to understand the implications of genetic change on how species interact and coexist. Our findings show that the current loss of genetic diversity may have cascading effects that lead to abrupt and catastrophic shifts in the persistence and functioning of terrestrial ecosystems," says Barbour. Story Source: Materials provided by University of Zurich. Note: Content may be edited for style and length. Journal Reference:
Proof of The Nash Equilibrium
In nature, organisms often support each other in order to gain an advantage. However, this kind of cooperation contradicts the theory of evolution proposed by Charles Darwin: Why would organisms invest valuable resources to help others? Instead, they should rather use them for themselves, in order to win the evolutionary competition with other species. A new study led by Prof. Dr. Christian Kost from the Department of Ecology at the Osnabrueck University now solved this puzzle. The results of the study were published in the scientific journal Current Biology. The research project was performed in collaboration with the Max Planck Institute for Chemical Ecology in Jena. Interactions between two or more organisms, in which all partners involved gain an advantage, are ubiquitous in nature and have played a key role in the evolution of life on Earth. For example, root bacteria fix nitrogen from the atmosphere, thus making it available to plants. In return, the plant supplies its root bacteria with nutritious sugars. However, it is nevertheless costly for both interaction partners to support each other. For example, the provision of sugar requires energy, which is then not available to the plant anymore. From this results the risk of cheating interaction partners that consume the sugar without providing nitrogen in return. The research team led by Prof. Dr. Christian Kost used bacteria as a model system to study the evolution of mutual cooperation. At the beginning of the experiment, two bacterial strains could only grow when they provided each other with essential amino acids. Over the course of several generations, however, the initial exchange of metabolic byproducts developed into a real cooperation: both partners increased the production of the exchanged amino acids in order to benefit their respective partner. Even though the increased amino acid production enhanced growth when both partners were present, it was extremely costly when individual bacterial strains had to grow without their partner. The observed changes were caused by the fact that individual bacterial cells had assembled into multicellular clusters. In these cell groups, cooperative mutants were rewarded. The more resources they invested in the growth of other cells, the more nutrients they received in return from their partners. "This kind of feedback represents a previously unknown mechanism, which promotes the evolution of cooperative interactions between two different organisms," says Prof. Dr. Christian Kost, leader of the study. Although the study was performed with bacteria in a test tube, the mechanism discovered can most likely explain the evolution of cooperation in many different ecological interactions. Story Source: Materials provided by Max Planck Institute for Chemical Ecology. Note: Content may be edited for style and length. Journal Reference:
re to edit. The Nash Equilibrium and Genomic Plasticity Survival of the Friendliest. It’s time to give the violent metaphors of evolution a break. Violence has been the sire of all the world’s values,” wrote poet Robinson Jeffers in 1940. “What but the wolf’s tooth whittled so fine the fleet limbs of the antelope? What but fear winged the birds, and hunger jeweled with such eyes the great goshawk’s head?” We’ve taken these metaphors for evolution to heart, reading them to mean that life is a race to kill or be killed. “Darwinian” stands in for “cutthroat,” “survival of the fittest” signifies survival of the ruthless. We see selective pressures that hone each organism for success and drive genetic innovation as the natural order of things. Two Models of Evolution: The early interpretation of Darwinian evolution as life-or-death contest is being complemented by an understanding of the importance of cooperation. But we know now that that picture is incomplete. Evolutionary progress can be propelled both by the competitive struggle to adapt to an environment, and by the relaxation of selective forces. When natural selection on an organism is relaxed, the creative powers of mutation can be unshackled and evolution accelerated. The relief of an easier life can inspire new biological forms just as powerfully as the threat of death. One of the best ways to relax selective forces is to work together, something that mathematical biologist Martin Nowak has called the “snuggle for survival.” New research has only deepened and broadened the importance of cooperation and lifting of selective pressures. It’s a big, snuggly world out there. *** The fitness of a species can be thought of as a multi-dimensional landscape defined by its compatibility with its environment. The species’ place within that landscape is determined by parameters like its fertility, metabolism, strength, and so on. A “peak” in this landscape represents a place in parameter space where a species’ fitness is high, a “valley” where it could be on the brink of extinction. The slopes of the features are also important. A broad, gentle hill in the fitness landscape would represent an area where the population could mutate and still survive; a narrow ridge would indicate a razor-thin set of possibilities, where even a small change could plunge an individual with a new mutation off a cliff. When selection is relaxed, the fitness landscape itself changes, such that thin precipices broaden out to plateaus. Once a selective constraint is lifted off a trait, the population is able to explore a wider array of possibilities in related traits, and evolution may improvise more freely. Selection can be relaxed by environmental factors, like a drop in predator numbers. But populations can also relax selection on themselves through their own behavior. A 2017 study conducted by researchers at the University of Sheffield tried to untangle the interplay between behavior and evolution by looking at a decidedly simple behavior in mice: huddling for warmth. The scientists simulated a population of mice, specifying their insulation and metabolic rate, and whether they were loners or huddlers. They tasked an evolutionary algorithm to optimize each population’s metabolic cost while maintaining an ideal temperature range. The harsh environment didn’t drive the evolution of the behaviors—the behaviors enabled the colonization of harsh environments. In the case of loners, the solution space allowing mice to efficiently maintain adequate temperatures was tiny. This is doubly problematic for a species. First, if the viable solution space is restricted, it’s much harder for evolution’s random walk to strike upon—“like finding a needle in a haystack.” And secondly, once a solution is found, it’s harder to explore subsequent, potentially beneficial mutations. When a species is inching along a narrow ridge in the fitness landscape, any false step could push it toward extinction. In the researchers’ model, huddling for warmth served to relax selection on the animal’s insulation, allowing genes controlling their metabolism to vary more without compromising their ability to maintain an optimal temperature. This softened the fitness peak, so that successive generations could rapidly explore a broad swath of the fitness landscape and accumulate a greater variety of mutations, providing a richer gene pool that might later be selected for in future times of environmental change. Of course, relaxing selection can also serve to increase the load of potentially deleterious mutations, so there is a tradeoff. But when selection is relaxed and populations are freer to explore the fitness landscape, they may stumble on large adaptive innovations faster. The authors draw a parallel with the evolution of warm-blooded animals from cold-blooded reptiles. It seems likely that an offshoot of reptiles evolved an insulating factor serving to relax selection—like fur or large body mass—before they began maintaining high body temperatures. Small warm-blooded animals face a great metabolic challenge, as their ratio of surface area to volume is so high that they radiate an enormous amount of heat. Once insulation was in place, the metabolism of proto-mammals was freer to mutate and hit upon stable body temperatures. And when they “discovered” warm-bloodedness, they realized a massive advantage: The first mammals could reliably hunt and forage at night, opening entirely new niches and ultimately resulting in a wildly successful class of animals. The authors argue that by huddling, mice effectively form a “super organism”—sharing heat to behaviorally approximate the benefits inherent to larger organisms without having to evolve a larger body, allowing their metabolism more freedom to change. Of course, computational studies must be taken with a grain of salt—given any model’s requisite assumptions and simplifications—though they allow us to simulate experiments that would take millennia to unfold in nature. By studying the phylogenetic history of related species, we can begin to correlate the interplay of behaviors with evolutionary dynamics in the real world. In 2017, scientists from Lund University, in Sweden, analyzed the breeding strategies of 4,000 bird species, tracking their movements into new ecosystems using known genetic relationships between the birds. It’s long been known that cooperative-breeding strategies are common in harsh environments. The assumption was that difficult conditions encouraged species to evolve sociable behaviors (at least toward relatives). But what if this presumed causality had it backward? By analyzing the historical migrations of birds, the researchers discovered that species that had already evolved cooperative behaviors in a benign environment were twice as likely to have moved into a harsh one than non-cooperative breeders. The researchers speculate that cooperation buffers against unpredictable breeding seasons, allowing already social populations to be more successful in invading new niches. The harsh environment didn’t drive the evolution of the behaviors—the behaviors enabled the colonization of harsh environments. *** We tend to conceive of life as separate from its habitat: The environment is a kind of container, and life is like a liquid that adapts to fill it. Sir Arthur Tansley introduced the concept of the ecosystem in 1935. He believed nature operated like a machine, and so, like an engineer, sought to map the flow of energy and matter through life and its environment. But an ecological niche is not, as I’d gathered from building shoebox dioramas in second grade, the raw physical parameters of an animal’s environment: salinity, alkalinity, humidity, temperature. It’s a web of relations, not just between a species and its habitat, but also with all the other species co-existing in the same space. A niche is no less dynamic than evolution is, contrary to Tansley’s mechanistic vision. “Palaeontologists often say that a burst of diversity in the fossil record simply ‘filled in ecological space,’ as if each new species simply took up residence in a square of a pre-existing chessboard,” writes paleobiologist Douglas Erwin. He suggests that a better analogy is that species build the chessboard themselves. Corals, for example, form their own protective niche by building reefs, which slow currents and reduce erosion on themselves. Reefs also serve to house countless other species, many of which have in turn evolved behaviors to protect corals. If an organism can modify its niche—by altering itself or its relationships with other species—it has the chance to build the world in which its future progeny will evolve, reshaping it to better ensure their survival. Evolution is not a weapons race, but a peace treaty among interdependent nations. One striking example of this kind of relationship emerged as a mystery during the dawn of microbiology. In the 19th century, bacteriologists cultured microbes using what was, at the time, cutting-edge technology: a warm vat of meat juice. Physician Robert Koch recognized that such broths likely harbored many different bacterial strains, and he surmised that if the bacteria were given a solid medium on which to grow, different colonies might be separated from each other and studied individually. He split a potato with a sterilized knife and smeared scrapings from an ill patient’s lesions onto it, creating the first solid culture. As different colonies formed, he isolated each onto a separate potato slice, but only a fraction of the divided strains survived alone. It’s now estimated that 98 percent of bacterial species cannot be singly cultured in a lab, a constraint that is not a purely academic problem: It’s massively hampered the discovery of new biomedical compounds. Our best antibiotics have been stolen from bacteria themselves; after millions of years of co-evolution, many bacteria have evolved highly effective poisons to thwart one another. But if we can’t grow most strains in labs, we can’t isolate the potentially useful compounds they produce. Until 2015, we hadn’t discovered a new class of antibiotic since 1987, and because bacteria evolve so rapidly, many have grown resistant to the antibiotics we’ve employed the past 30+ years. There are doubtless many reasons bacteria resist lab life, but chief among them is the fact that, in the wild, bacteria are not self-sufficient: They’ve co-evolved to depend on each other. It may seem precarious, from the vantage point of natural selection, for species to require each other to survive, but the overwhelming ubiquity of interdependence suggest it must have serious advantages. The Black Queen Hypothesis describes one such possibility. In the Black Queen model, organisms shed genes coding for functions that other species in the environment already provide. It’s a foil to the better-known Red Queen hypothesis, which posits that organisms are subject to a sort of evolutionary arms race, ever adapting new weapons and defenses just to avoid extinction. Though evolution is often characterized as a forward march of complexity, organisms actually shed genes quite often. Biological functions are metabolically costly to maintain, and if they aren’t strictly necessary, they’re best excluded from a genome. (The Black Queen Hypothesis takes its name from the game of Hearts, wherein players try to avoid picking up the queen of spades to avoid a particularly heavy penalty.) A canonical illustration of the Black Queen Hypothesis is found in two free-floating marine cyanobacteria, Synechococcus and Prochlorococcus. They use photosynthesis to feed themselves but are both harmed by a toxic byproduct of the process, hydrogen peroxide. An enzyme that can neutralize hydrogen peroxide, catalase peroxidase, is particularly costly to produce. And, though both need it to survive, only Synechococcus carries the genes for it. Synechococcus mops up all the hydrogen peroxide in the environment, while Prochlorococcus enjoys protection at an energetic discount. Helper species like Synechococcus can become keystone species in an ecosystem. Because they provide a common good necessary for many species, they may come to be shielded from competition by the species that rely on them, as happens with corals. The success of Prochlorococcus is directly dependent on the relative abundance of Synechococcus. If it begins to outgrow its helper, its numbers will be culled by an increase in hydrogen peroxide. The chessboard has changed: Existence is not a zero-sum game. Shedding the genes for catalase peroxidase confers a substantial energetic benefit to Prochlorococcus, and, as we’ve seen, relaxing selection on a species may allow it to explore new functions in other realms. Evolution at Work: Technology that enables cooperation has accelerated the evolution of our species. Long periods of harmonious co-existence may be the evolutionary precursor for true symbiotic relationships. Billions of years ago, another ancient cyanobacteria was engulfed and “domesticated” by an ancestor of plants. It shed most of the genes it needed for an independent existence and became what we now know as the chloroplast. In return for a safe environment, these chloroplasts performed photosynthesis for their hosts, fueling a new form of life that eventually spread over much of the Earth. It’s likely this same kind of division of labor was a seed for the development of multicellular organisms. Here, evolution is not a weapons race, but a peace treaty among interdependent nations. *** You and I may never have evolved if it weren’t for relaxed selection. Humans have created a unique global niche where we are largely shielded from selective forces: Agriculture staves off starvation, medicine protects us from disease, cultural norms promote group harmony. Our evolution has been profoundly influenced by our selection-buffering behaviors. For instance, the appearance of some modern human features appears to be correlated with a rise in energy consumption, linked to the introduction of meat in our diet. Our ancestor Homo erectus began eating significantly more meat than its predecessors, yet its jaws and teeth were made for crushing tough plant matter and ill-adapted for chewing flesh. This species, it seems, was using tools not only to hunt but also to process meat (and, possibly, using fire to cook it). Energy-rich meat relaxed selection on our metabolism and digestive system—we could devote tenfold less time to chewing vegetation—which paved the way for our modern physiology. Our teeth, jaws, and guts shrank, allowing more energy to be allocated to our swelling brains, which necessitated a protracted, calorie-rich childhood to fully develop. Armed with crude but effective hand axes, Homo erectus shifted its evolutionary destiny. In humans and other animals that learn socially, selection buffering is especially powerful: Adaptive habits, like huddling for warmth and using tools to prepare food, can sweep through a population much faster than genomic changes. Our genomes continue to be affected by culture to this day. Take the lactase gene, which codes for the enzyme that digests lactose in milk. While it’s present in all human genomes, it has traditionally been turned off after infancy, when children stop nursing. But relatively recently in our natural history, several different groups that farmed cattle evolved the ability to digest lactose throughout their lives, enabling access to a new, valuable form of nutrition. Today it is the descendants of those groups who can drink milk as adults without ill effects. As humans collected into ever larger groups, the discovery of increasingly complex technology was accelerated. In high-density settlements, artisans and innovators could specialize in their crafts and exchange ideas. Selection for tool development has had an associated pressure on our ability to co-exist peacefully in large numbers, and aggressive, uncooperative individuals may have been selected against. We’ve become, by most accounts, a gentler, more cooperative species over time. Our testosterone levels, for instance, appear to have dropped, judging by the brow size of our fossilized predecessors. Some scientists suggest that the emergence of complex human culture amounts to us having, effectively, domesticated ourselves. For those most invested in the old-school Darwinian view of the survival of the fittest and violence as virtue, then, the message is clear: Just relax. Kelly Clancy studies neuroscience as a postdoctoral fellow at the University of Basel, in Switzerland. Previously, she roamed the world as an astronomer and served with the Peace Corps in Turkmenistan. She won the 2014 Regeneron Prize for Creative Innovation for her work designing drug-free brain therapies This article was originally published on March 23, 2017, by Nautilus, and is republished here with permission. Transposons Creating Gene Networks the same way that Lego pieces can be arranged in new ways to build a variety of structures, genetic elements can be mixed and matched to create new genes, according to new research. A long-proposed mechanism for creating genes, called exon shuffling, works by shuffling functional blocks of DNA sequences into new genes that express proteins. A study, "Recurrent Evolution of Vertebrate Transcription Factors by Transposase Capture," published Feb. 19 in Science, investigates how genetic elements called transposons, or "jumping genes," are added into the mix during evolution to assemble new genes through exon shuffling. Transposons, first discovered in the 1940s by Cornell alum and Nobel Prize-winner Barbara McClintock '23, M.A. '25, Ph.D. '27, are abundant components of genomes -- they make up half of human DNA -- and have the ability to hop and replicate selfishly in the genome. Some transposons contain their own genes that code for enzymes called transposase proteins, which cut and paste genetic material from one chromosomal location to another. The study, which focused on tetrapods (four-limbed vertebrates), is important because it shows that transposons represent an important force in the creation of new genes during evolution. The work also explains how genes critical for human development were born. "We think it's very likely this mechanism may extend beyond vertebrates and could be more of a fundamental mechanism that occurs in non-vertebrates as well," said first author Rachel Cosby, Ph.D. '19, a postdoctoral researcher at the National Institutes of Health. Cosby is a former graduate student in the lab of senior author Cedric Feschotte, professor in the Department of Molecular Biology and Genetics in the College of Agriculture and Life Sciences. "You are putting the bricks in in a different way and you construct a whole new thing," Feschotte said. "We are looking at the question of how genes are born. The originality is that we are looking at the role of transposons in creating proteins with novel function in evolution." In the study, the researchers first mined existing databases for genomes of tetrapods, because genomes for more than 500 species have been fully sequenced. Cosby and colleagues searched for combinations of DNA sequences known to be characteristic of transposons fused to host sequences to find good candidates for study. They then chose genes that evolved relatively recently -- within tens of millions of years ago -- so they could trace the history of the gene's development through the vertebrate tree of life. Though genes fused with these transposases are relatively rare, the researchers found them all over the vertebrate tree of life. The researchers identified more than 100 distinct genes fused with transposases born in the past 350 million years along different species lineages, including genes in birds, reptiles, frogs, bats and koalas, and a total of 44 genes born this way in the human genome. Cosby and colleagues selected four recently evolved genes and performed a wide range of experiments in cell culture to understand their functions. They found the proteins derived from these genes are able to bind to specific DNA sequences and turn off gene expression. Such genes are known as transcription factors and act as master regulator genes for development and basic physiology. One such gene, PAX6, is well studied, plays a key role as a master regulator in the formation of eyes in all animals and is highly conserved throughout evolution. "If you put a PAX6 gene from a mouse into a Drosophila [fruit fly], it works," Feschotte said. Though others have proposed before that PAX6 is derived from a transposase fusion, the researchers in this study further validated the hypothesis. Cosby and colleagues isolated one of these recently evolved genes in bats, called KRABINER, and then used CRISPR gene-editing technology to delete it from the bat genome and see what genes were affected, before adding it back in. The experiment revealed that when KRABINER was removed, hundreds of genes were dysregulated, and when they restored it, normal functioning returned. The protein expressed by the KRABINER gene bound to other related transposons in the bat genome, Cosby said. "The experiment revealed that it controls a large network of other genes wired through the past dispersion of related transposons throughout the bat genome -- creating not just a gene but what is known as a gene regulatory network," Feschotte said. Current and former Feschotte lab members Julius Judd, Ruiling Zhang '20, Alan Zhong '19, Nathaniel Garry '21 and collaborator Ellen Pritham are co-authors of the paper. The study was funded by the National Institutes of Health. Story Source: Materials provided by Cornell University. Original written by Krishna Ramanujan. Note: Content may be edited for style and length. Journal Reference:
Cite This Page: Cornell University. "'Jumping genes' repeatedly form new genes over evolution." ScienceDaily. ScienceDaily, 22 February 2021. <www.sciencedaily.com/releases/2021/02/210222124540.htm>.ere to edit. Genomic Pasticity in Adaptation
There's a paradox within the theory of evolution: The life forms that exist today are here because they were able to change when past environments disappeared. Yet, organisms evolve to fit into specific environmental niches. "Ever-increasing specialization and precision should be an evolutionary dead end, but that is not the case. How the ability to fit precisely into a current setting is reconciled with the ability to change is the most fundamental question in evolutionary biology," says Alex Badyaev, a University of Arizona professor of ecology and evolutionary biology . Badyaev is co-author of a paper published in Nature Communications that suggests an explanation based on the evolution of colorful pigments in bird feathers throughout North America. He wrote the paper with two former graduate students -- lead author Ahva Potticary, now a UArizona lecturer, and Erin Morrison, now an assistant professor at New York University. There are two general possible solutions, according to Badyaev. First, the mechanisms that enable organisms to fit well into their current environment and the mechanisms that enable change in adaptations are distinct -- the latter are suppressed as organisms fit better and better into their current setting and activated only when the environment changes. The second is that the mechanisms that make organisms fit into current environments are themselves modified during evolution. "Distinguishing between these possibilities is challenging because in evolutionary biology we necessarily study processes that occurred in the past, the events that we missed," he said. "So, instead, we infer what we missed from comparisons of species that exist today. Although this approach can tell us how well the current organisms fit into their current environment, it cannot tell us how they got here." Ultimately, the first scenario was supported by the researchers' work. The mechanisms that make organisms locally fit and those responsible for change are distinct and occur sequentially in evolution. Carotenoid Clues Badyaev and his team aimed to directly observe adaptation to new environments in action while specifically paying attention to the mechanisms involved. The opportunity was provided by the house finch, a ubiquitous Sonoran Desert bird that over the last century has spread throughout most of North America and now occupies the largest ecological ranges of any living bird species. Birds color themselves by eating and integrating pigmented molecules called carotenoids into their feathers. "Carotenoids are large molecules, and stuffing them into growing feather is a messy process, resulting in all kinds of structural modifications and aberrations to feathers," Badyaev said. "This presents a unique opportunity to study how well-characterized developmental mechanisms that produce an intricate feather co-evolve with unpredictable external inputs needed to color them." In feathers where structural integrity is essential, such as in temperature-regulating down or flight feathers, mechanisms evolve that buffer feather growth from incorporating carotenoids. For this reason, flight feathers or down feathers are almost never colorful in any bird species. On the opposite end of spectrum, ornamental feathers benefit from being colorful and evolve mechanisms that modify their structure to enable greater incorporation of carotenoids and to enhance their presentation. The authors took advantage of this diversity and studied how this array of mechanisms -- from complete buffering of carotenoids to fully embracing them -- actually evolves. The sources of carotenoid pigments differ across the house finch's huge range. In native desert populations, finches obtain their pigments from cactus pollen and fruits, while in urban populations they get them from newly introduced plant species and bird feeders. In northern populations, they incorporate the pigments from grass seeds, buds and berries. "As expected, within each of these locations finches have evolved precise adaptations to incorporate diverse local carotenoids into their feathers," Badyaev said. But the unique aspect of this study is that "we knew the colonization routes of these birds, which enabled us to observe how they modify these adaptations as they move from one location to the next over the last century." This approach not only allowed the team to directly study the process of evolution but also enabled them to study repeated evolution in the wild, because birds evolved distinct local adaptations in parallel from known starting points as they spread through the continent. "We got to replay the tape of evolution of this adaptation, instead of deducing the process from the outcome," Badyaev said. The team established 45 study populations along colonization routes that the species took from its native southern Arizona to the northwestern United States. They also explored how species changed within regions, such as between Arizona desert populations and urban populations on the University of Arizona campus and in Tucson. In all of these populations they examined microscopic structure and complete carotenoid composition in thousands upon thousands of feather samples. The unprecedented scale and depth of the study -- believed to be the largest of its kind in a wild bird species -- led to two discoveries. First, evolution proceeded by remarkably similar sequences from widely diverse starting points. Unfamiliar local carotenoids exerted major modifications in developing feathers at first, but the longer birds persisted in a region and the more familiar they became with local carotenoids, the better there were able to incorporate them into their feathers, eventually evolving precise local adaptations. Second, and most importantly, although carotenoids and their mixtures differed strongly between locations as distinct as deserts and northern evergreen forests, the mechanisms behind their incorporation into growing feathers were remarkably uniform and not specific to biochemical properties of individual carotenoid compounds. Instead, in all populations, evolution resulted from changes in mechanisms that buffered previous local adaptation from external stressors. These general stress-buffering mechanisms -- what Badyaev called "the guardians of local adaptations" -- had to be recruited to allow evolution of new adaptations. In other words, "the boundaries of current adaptations become bridges between successive adaptions in evolution," Badyaev said. The next step for the authors is to study the origin of molecular and developmental mechanisms they implicated in stress-buffering processes in evolution. Story Source: Materials provided by University of Arizona. Note: Content may be edited for style and length. Journal Reference:
PROOF THAT GENOMIC CHANGE OCCURS BEFORE THEY HAVE ADAPTIVE ADVANTAGE
February 5, 2021 Source: University of Copenhagen - Faculty of Science Summary: Lungs and limbs have been thought of as key innovations that came with the vertebrate transition from water to land. But in fact, the genetic basis of air-breathing and limb movement was already established in our fish ancestor 50 million years earlier, according to a recent genome mapping of primitive fish. The new study changes our understanding of a key milestone in our own evolutionary history. Share: FULL STORY People traditionally think that lungs and limbs are key innovations that came with the vertebrate transition from water to land. But in fact, the genetic basis of air-breathing and limb movement was already established in our fish ancestor 50 million years earlier. This, according to a recent genome mapping of primitive fish conducted by the University of Copenhagen, among others. The new study changes our understanding of a key milestone in our own evolutionary history. There is nothing new about humans and all other vertebrates having evolved from fish. The conventional understanding has been that certain fish shimmied landwards roughly 370 million years ago as primitive, lizard-like animals known as tetrapods. According to this understanding, our fish ancestors came out from water to land by converting their fins to limbs and breathing under water to air-breathing. However, limbs and lungs are not innovations that appeared as recent as once believed. Our common fish ancestor that lived 50 million years before the tetrapod first came ashore already carried the genetic codes for limb-like forms and air breathing needed for landing. These genetic codes are still present in humans and a group of primitive fishes. This has been demonstrated by recent genomic research conducted by University of Copenhagen and their partners. The new research reports that the evolution of these ancestral genetic codes might have contributed to the vertebrate water-to-land transition, which changes the traditional view of the sequence and timeline of this big evolutionary jump. The study has been published in the scientific journal Cell. "The water-to-land transition is a major milestone in our evolutionary history. The key to understanding how this transition happened is to reveal when and how the lungs and limbs evolved. We are now able to demonstrate that the genetic basis underlying these biological functions occurred much earlier before the first animals came ashore," stated by professor and lead author Guojie Zhang, from Villum Centre for Biodiversity Genomics, at the University of Copenhagen's Department of Biology. A group of ancient living fishes might hold the key to explain how the tetrapod ultimately could grow limbs and breathe on air. The group of fishes includes the bichir that lives in shallow freshwater habitats in Africa. These fishes differ from most other extant bony fishes by carrying traits that our early fish ancestors might have had over 420 million years ago. And the same traits are also present in for example humans. Through a genomic sequencing the researchers found that the genes needed for the development of lungs and limbs have already appeared in these primitive species. Our synovial joint evolved from fish ancestor Using pectoral fins with a locomotor function like limbs, the bichir can move about on land in a similar way to the tetrapod. Researchers have for some years believed that pectoral fins in bichir represent the fins that our early fish ancestors had. The new genome mapping shows that the joint which connects the socalled metapterygium bone with the radial bones in the pectoral fin in the bichir is homologous to synovial joints in humans -- the joints that connect upper arm and forearm bones. The DNA sequence that controls the formation of our synovial joints already existed in the common ancestors of bonefish and is still present in these primitive fishes and in terrestrial vertebrates. At some point, this DNA sequence and the synovial joint was lost in all of the common bony fishes -- the socalled teleosts. "This genetic code and the joint allows our bones move freely, which explains why the bichir can move around on land," says Guojie Zhang. First lungs, then swim bladder Moreover, the bichir and a few other primitive fishes have a pair of lungs that anatomically resembles ours. The new study reveals that the lungs in both bichir and alligator gar also function in a similar manner and express same set of genes as human lungs. At the same time, the study demonstrates that the tissue of the lung and swim bladder of most extant fishes are very similar in gene expression, confirming they are homologous organs as predicted by Darwin. But while Darwin suggested that swim bladders converted to lungs, the study suggests it is more likely that swim bladders evolved from lungs. The research suggests that our early bony fish ancestors had primitive functional lungs. Through evolution, one branch of fish preserved the lung functions that are more adapted to air breathing and ultimately led to the evolution of tetrapods. The other branch of fishes modified the lung structure and evolved with swim bladders, leading the evolution of teleosts. The swim bladders allow these fishes to maintain buoyancy and perceive pressure, thus better survive under water. "The study enlightens us with regards to where our body organs came from and how their functions are decoded in the genome. Thus, some of the functions related to lung and limbs did not evolve at the time when the water-to-land transition occurred, but are encoded by some ancient gene regulatory mechanisms that were already present in our fish ancestor far before landing. It is interesting that these genetic codes are still present in these 'living-fossil'' fishes, which offer us the opportunity to trace back the root of these genes," concludes Guojie Zhang. FACT BOX 1: Not just limbs and lungs, but also the heart Primitive fish and humans also share a common and critical function in the cardio-respiratory system: The conus arteriosus, a structure in the right ventricle of our heart which might allow the heart to efficiently deliver the oxygen to the whole body, and which is also found in the bichir. However, the vast majority of bony fish have lost this structure. The researchers discovered a genetic element that appears to control the development of the conus arteriosus. Transgenic experiments with mice showed that when researchers removed this genetic element, the mutated mice died due to thinner, smaller right ventricles, which lead to congenital heart defects and compromised heart function. FACT BOX 2:
Story Source: Materials provided by University of Copenhagen - Faculty of Science. Note: Content may be edited for style and length. Journal References:
Cite This Page: University of Copenhagen - Faculty of Science. "We're more like primitive fishes than once believed, new research shows." ScienceDaily. ScienceDaily, 5 February 2021. <www.sciencedaily.com/releases/2021/02/210205210627.htm>. Scientists Seek to Update Evolution Recent discoveries have led some researchers to argue that the modern evolutionary synthesis needs to be amended. 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 ItEvery 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. Audience members at the Royal Society’s “New Trends in Evolutionary Biology” conference. Tom Parker for Quanta Magazine 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 DarwinEva Jablonka, a biologist at Tel Aviv University, used her talk to explore the evidence for a form of heredity beyond genes. Our cells use a number of special molecules to control which of their genes make proteins. In a process called methylation, for example, cells put caps on their DNA to keep certain genes shut down. When cells divide, they can reproduce the same caps and other controls on the new DNA. Certain signals from the environment can cause cells to change these so-called “epigenetic” controls, allowing organisms to adjust their behavior to new challenges. Some studies indicate that — under certain circumstances — an epigenetic change in a parent may get passed down to its offspring. And those children may pass down this altered epigenetic profile to their children. This would be kind of heredity that’s beyond genes. The evidence for this effect is strongest in plants. In one study, researchers were able to trace down altered methylation patterns for 31 generations in a plant called Arabidopsis. And this sort of inheritance can make a meaningful difference in how an organism works. In another study, researchers found that inherited methylation patterns could change the flowering time of Arabidopsis, as well as the size of its roots. The variation that these patterns created was even bigger than what ordinary mutations caused. After presenting evidence like this, Jablonka argued that epigenetic differences could determine which organisms survived long enough to reproduce. “Natural selection could work on this system,” she said. While natural selection is an important force in evolution, the speakers at the meeting presented evidence for how it could be constrained, or biased in a particular direction. Gerd Müller, a University of Vienna biologist, offered an example from his own research on lizards. A number of species of lizards have evolved feet that have lost some toes. Some have only four toes, while others have just one, and some have lost their feet altogether. Sonia Sultan has shown that genetically identical organisms can be raised in such a way that they appear to be completely separate species. Tom Parker for Quanta Magazine The Modern Synthesis, Müller argued, leads scientists to look at these arrangements as simply the product of natural selection, which favors one variant over others because it has a survival advantage. But that approach doesn’t work if you ask what the advantage was for a particular species to lose the first toe and last toe in its foot, instead of some other pair of toes. “The answer is, there is no real selective advantage,” said Müller. The key to understanding why lizards lose particular toes is found in the way that lizard embryos develop toes in the first place. A bud sprouts off the side of the body, and then five digits emerge. But the toes always appear in the same sequence. And when lizards lose their toes through evolution, they lose them in the reverse order. Müller suspects this constraint is because mutations can’t create every possible variation. Some combinations of toes are thus off-limits, and natural selection can never select them in the first place. Development may constrain evolution. On the other hand, it also provides animals and plants with remarkable flexibility. Sonia Sultan, an evolutionary ecologist from Wesleyan University, offered a spectacular case in point during her talk, describing a plant she studies in the genus Polygonum that takes the common name “smartweed.” The Modern Synthesis, Sultan said, would lead you to look at the adaptations in a smartweed plant as the fine-tuned product of natural selection. If plants grow in low sunlight, then natural selection will favor plants with genetic variants that let them thrive in that environment — for example, by growing broader leaves to catch more photons. Plants that grow in bright sunlight, on the other hand, will evolve adaptations that let them thrive in those different conditions. “It’s a commitment to that view that we’re here to confront,” Sultan said. If you raise genetically identical smartweed plants under different conditions, Sultan showed, you’ll end up with plants that may look like they belong to different species. For one thing, smartweed plants adjust the size of their leaves to the amount of sunlight they get. In bright light, the plants grow narrow, thick leaves, but in low light, the leaves become broad and thin. In dry soil, the plants send roots down deep in search of water, while in flood soil, they grow shallow hairlike roots that that stay near the surface. Scientists at the meeting argued that this flexibility — known as plasticity — can itself help drive evolution. It allows plants to spread into a range of habitats, for example, where natural selection can then adapt their genes. And in another talk, Susan Antón, a paleoanthropologist at New York University, said that plasticity may play a significant role in human evolution that’s gone underappreciated till now. That’s because the Modern Synthesis has strongly influenced the study of human evolution for the past half century. Paleoanthropologists tended to treat differences in fossils as the result of genetic differences. That allowed them to draw an evolutionary tree of humans and their extinct relatives. This approach has a lot to show for it, Antón acknowledged. By the 1980s, scientists had figured out that our early ancient relatives were short and small-brained up to about two million years ago. Then one lineage got tall and evolved big brains. That transition marked the origin of our genus, Homo. But sometimes paleoanthropologists would find variations that were harder to make sense of. Two fossils might look in some ways like they should be in the same species but look too different in other respects. Scientists would usually dismiss those variations as being caused by the environment. “We wanted to get rid of all that stuff and get down to their essence,” Antón said. Andy Whiten, who studies the evolution of social learning and culture at the University of St. Andrews, takes it all in. Tom Parker for Quanta Magazine But that stuff is now too abundant to ignore. Scientists have found a dizzying variety of humanlike fossils dating back to 1.5 to 2.5 million years ago. Some are tall, and some are short. Some have big brains and some have small ones. They all have some features of Homo in their skeleton, but each has a confusing mix-and-match assortment. Antón thinks that the Extended Evolutionary Synthesis can help scientists make sense of this profound mystery. In particular, she thinks that her colleagues should take plasticity seriously as an explanation for the weird diversity of early Homo fossils. To support this idea, Antón pointed out that living humans have their own kinds of plasticity. The quality of food a woman gets while she’s pregnant can influence the size and health of her baby, and those influences can last until adulthood. What’s more, the size of a woman — influenced in part by her own mother’s diet — can influence her own children. Biologists have found that women with longer legs tend to have larger children, for example. Antón proposed that the weird variations in the fossil record might be even more dramatic examples of plasticity. All these fossils date to when Africa’s climate fell into a period of wild climate swings. Droughts and abundant rains would have changed the food supply in different parts of the world, perhaps causing early Homo to develop differently. The Extended Evolutionary Synthesis may also help make sense of another chapter in our history: the dawn of agriculture. In Asia, Africa and the Americas, people domesticated crops and livestock. Melinda Zeder, an archaeologist at the Smithsonian Institution, gave a talk at the meeting about the long struggle to understand how this transformation unfolded. Before people farmed, they foraged for food and hunted wild game. Zeder explained how many scientists treat the behavior of the foragers in a very Modern Synthesis way: as finely tuned by natural selection to deliver the biggest payoff for their effort to find food. The trouble is that it’s hard to see how such a forager would ever switch to farming. “You don’t get the immediate gratification of grabbing some food and putting it in your mouth,” Zeder told me. Some researchers suggested that the switch to agriculture might have occurred during a climate shift, when it got harder to find wild plants. But Zeder and other researchers have actually found no evidence of such a crisis when agriculture arose. Zeder argues that there’s a better way of thinking about this transition. Humans are not passive zombies trying to survive in a fixed environment. They are creative thinkers who can change the environment itself. And in the process, they can steer evolution in a new direction. Scientists call this process niche construction, and many species do it. The classic case is a beaver. It cuts down trees and makes a dam, creating a pond. In this new environment, some species of plants and animals will do better than others. And they will adapt to their environment in new ways. That’s true not just for the plants and animals that live around a beaver pond, but for the beaver itself. When Zeder first learned about niche construction, she says, it was a revelation. “Little explosions were going off in my head,” she told me. The archaeological evidence she and others had gathered made sense as a record of how humans changed their own environment. Early foragers show signs of having moved wild plants away from their native habitats to have them close at hand, for example. As they watered the plants and protected them from herbivores, the plants adapted to their new environment. Weedy species also moved in and became crops of their own. Certain animals adapted to the environment as well, becoming dogs, cats and other domesticated species. Denis Noble now sees a need for an Extended Evolutionary Synthesis. Tom Parker for Quanta Magazine Gradually, the environment changed from sparse patches of wild plants to dense farm fields. That environment didn’t just drive the evolution of the plants. It also began to drive the cultural evolution of the farmers, too. Instead of wandering as nomads, they settled down in villages so that they could work the land around them. Society became more stable because children received an ecological inheritance from their parents. And so civilization began. Niche construction is just one of many concepts from the Extended Evolutionary Synthesis that can help make sense of domestication, Zeder said. During her talk, she presented slide after slide of predictions it provides, about everything from the movements of early foragers to the pace of plant evolution. “It felt like an infomercial for the Extended Evolutionary Synthesis,” Zeder told me later with a laugh. “But wait! You can get steak knives!” The Return of Natural SelectionAmong the members of the audience was a biologist named David Shuker. After listening quietly for a day and a half, the University of St Andrews researcher had had enough. At the end of a talk, he shot up his hand. The talk had been given by Denis Noble, a physiologist with a mop of white hair and a blue blazer. Noble, who has spent most of his career at Oxford, said he started out as a traditional biologist, seeing genes as the ultimate cause of everything in the body. But in recent years he had switched his thinking. He spoke of the genome not as a blueprint for life but as a sensitive organ, detecting stress and rearranging itself to cope with challenges. “I’ve been on a long journey to this view,” Noble said. To illustrate this new view, Noble discussed an assortment of recent experiments. One of them was published last year by a team at the University of Reading. They did an experiment on bacteria that swim by spinning their long tails. First, the scientists cut a gene out of the bacteria’s DNA that’s essential for building tails. The researchers then dropped these tailless bacteria into a petri dish with a meager supply of food. Before long, the bacteria ate all the food in their immediate surroundings. If they couldn’t move, they died. In less than four days in these dire conditions, the bacteria were swimming again. On close inspection, the team found they were growing new tails. “This strategy is to produce rapid evolutionary genome change in response to the unfavorable environment,” Noble declared to the audience. “It’s a self-maintaining system that enables a particular characteristic to occur independent of the DNA.” That didn’t sound right to Shuker, and he was determined to challenge Noble after the applause died down. “Could you comment at all on the mechanism underlying that discovery?” Shuker asked. Noble stammered in reply. “The mechanism in general terms, I can, yes…” he said, and then started talking about networks and regulation and a desperate search for a solution to a crisis. “You’d have to go back to the original paper,” he then said. While Noble was struggling to respond, Shuker went back to the paper on an iPad. And now he read the abstract in a booming voice. “‘Our results demonstrate that natural selection can rapidly rewire regulatory networks,’” Shuker said. He put down the iPad. “So it’s a perfect, beautiful example of rapid neo-Darwinian evolution,” he declared. Shuker distilled the feelings of a lot of skeptics I talked to at the conference. The high-flying rhetoric about a paradigm shift was, for the most part, unwarranted, they said. Nor were these skeptics limited to the peanut gallery. Several of them gave talks of their own. “I think I’m expected to represent the Jurassic view of evolution,” said Douglas Futuyma when he got up to the podium. Futuyma is a soft-spoken biologist at Stony Brook University in New York and the author of a leading textbook on evolution. In other words, he was the target of many complaints during the meeting that textbooks paid little heed to things like epigenetics and plasticity. In effect, Futuyma had been invited to tell his colleagues why those concepts were ignored. “We must recognize that the core principles of the Modern Synthesis are strong and well-supported,” Futuyma declared. Not only that, he added, but the kinds of biology being discussed at the Royal Society weren’t actually all that new. The architects of the Modern Synthesis were already talking about them over 50 years ago. And there’s been a lot of research guided by the Modern Synthesis to make sense of them. Take plasticity. The genetic variations in an animal or a plant govern the range of forms into which organism can develop. Mutations can alter that range. And mathematical models of natural selection show how it can favor some kinds of plasticity over others. If the Extended Evolutionary Synthesis was so superfluous, then why was it gaining enough attention to warrant a meeting at the Royal Society? Futuyma suggested that its appeal was emotional rather than scientific. It made life an active force rather than the passive vehicle of mutations. “I think what we find emotionally or aesthetically more appealing is not the basis for science,” Futuyma said. Still, he went out of his way to say that the kind of research described at the meeting could lead to some interesting insights about evolution. But those insights would only arise with some hard work that leads to hard data. “There have been enough essays and position papers,” he said. Some members in the audience harangued Futuyma a bit. Other skeptical speakers sometimes got exasperated by arguments they felt didn’t make sense. But the meeting managed to reach its end on the third afternoon without fisticuffs. “This is likely the first of many, many meetings,” Laland told me. In September, a consortium of scientists in Europe and the United States received $11 million in funding (including $8 million from the John Templeton Foundation) to run 22 studies on the Extended Evolutionary Synthesis. Many of these studies will test predictions that have emerged from the synthesis in recent years. They will see, for example, if species that build their own environments — spider webs, wasp nests and so on — evolve into more species than ones that don’t. They will look at whether more plasticity allows species to adapt faster to new environments. “It’s doing the research, which is what our critics are telling us to do,” said Laland. “Go find the evidence.” Correction: An earlier version of this article misidentified the photograph of Andy Whiten as Gerd Müller. This article was reprinted on TheAtlantic.com. THE EXPERIMENTAL STUDIES
Darwin Proved Wrong about Fitness New microbial research at the University of Copenhagen suggests that 'survival of the friendliest' outweighs 'survival of the fittest' for groups of bacteria. Bacteria make space for one another and sacrifice properties if it benefits the bacterial community as a whole. The discovery is a major step towards understanding complex bacteria interactions and the development of new treatment models for a wide range of human diseases and new green technologies. New microbial research at the Department of Biology reveals that bacteria would rather unite against external threats, such as antibiotics, rather than fight against each other. The report has just been published in the scientific publication ISME Journal. For a number of years the researchers have studied how combinations of bacteria behave together when in a confined area. After investigating many thousands of combinations it has become clear that bacteria cooperate to survive and that these results contradict what Darwin said in his theories of evolution. "In the classic Darwinian mindset, competition is the name of the game. The best suited survive and outcompete those less well suited. However, when it comes to microorganisms like bacteria, our findings reveal the most cooperative ones survive," explains Department of Biology microbiologist, Professor Søren Johannes Sørensen. Social bacteria work shoulder to shoulder By isolating bacteria from a small corn husk (where they were forced to "fight" for space) the scientists were able to investigate the degree to which bacteria compete or cooperate to survive. The bacterial strains were selected based upon their ability to grow together. Researchers measured bacterial biofilm, a slimy protective layer that shields bacteria against external threats such as antibiotics or predators. When bacteria are healthy, they produce more biofilm and become stronger and more resilient. Time after time, the researchers observed the same result: Instead of the strongest outcompeting the others in biofilm production, space was allowed to the weakest, allowing the weak to grow much better than they would have on their own. At the same time the researchers could see that the bacteria split up laborious tasks by shutting down unnecessary mechanisms and sharing them with their neighbors. "It may well be that Henry Ford thought that he had found something brilliant when he introduced the assembly line and worker specialization, but bacteria have been taking advantage of this strategy for a billion years," says Søren Johannes Sørensen referring to the oldest known bacterial fossils with biofilm. He adds: "Our new study demonstrates that bacteria organize themselves in a structured way, distribute work and even to help each other. This means that we can find out which bacteria cooperate, and possibly, which ones depend on each another, by looking at who sits next to who." Understanding invisible bacterial synergy The researchers also investigated what properties bacteria had when they were alone versus when they were with other bacteria. Humans often discuss the work place or group synergy, and how people inspire each other. Bacteria take this one step further when they survive in small communities. "Bacteria take our understanding of group synergy and inspiration to a completely different level. They induce attributes in their neighbors that would otherwise remain dormant. In this way groups of bacteria can express properties that aren't possible when they are alone. When they are together totally new features can suddenly emerge," Søren Johannes Sørensen explains. Understanding how bacteria interact in groups has the potential to create a whole new area in biotechnology that traditionally strives to exploit single, isolated strains, one at a time. "Bio-based society is currently touted as a solution to model many of the challenges that our societies face. However, the vast majority of today's biotech is based on single organisms. This is in stark contrast to what happens in nature, where all processes are managed by cooperative consortia of organisms. We must learn from nature and introduce solutions to tap the huge potential of biotechnology in the future," according to Søren Johannes Sørensen. Story Source: Materials provided by University of Copenhagen. Note: Content may be edited for style and length. Journal Reference:
Ci Rapid Evolutionary Complexity
A team of scientists, led by Harvard researchers, has used a new method of DNA "re-barcoding" to track rapid evolution in yeast. The new approach, published in Nature, advances the field of organismic and evolutionary biology and holds promise for real-world results. The potential impact of the work can be illustrated using the example of flu vaccines. An accurate prediction of what strains of influenza will dominate over the next year is necessary to ensure the vaccines produced are useful. Such prediction relies on tracking evolution. "We have the sequence of all these flu strains, and we're watching their evolution. What you should be able to do is look at how they've evolved in the past and be able to predict into the future what is going to win and what is going to lose. The problem is, we don't know how to do that prediction," explained Michael Desai, Professor of Organismic and Evolutionary Biology (OEB) and of Physics at Harvard. Desai, in whose lab the study was conducted, said that the questions are basic: "There is this swarm of mutations that are constantly happening," he said. "How do they battle it out, and what determines who wins?" "We have been taught that evolution 'is slow' and involves the 'survival of the fittest,' added Alex N. Nguyen Ba, a post-doctoral fellow in Desai's lab. "It turns out that molecular evolution doesn't work that way. It's actually much faster than how we've been taught. This makes evolution way more complex than what has been anticipated." Nguyen Ba is one of three co-lead authors of the new study, along with Ivana Cvijović and José I. Rojas Echenique Such evolution has been posited mathematically over the past two decades. However, previous lab experiments have not been able to prove or disprove the theory. Rather, they have only been able to examine the process with high resolution over a short period of time, or with low resolution over a long period of time. Collectively, Desai explained, the paper's authors -- who include Katherine R. Lawrence of MIT and Harvard's Artur Rego-Costa, along with Xianan Liu of Stanford and Sasha F. Levy of SLAC National Accelerator Laboratory -- have done both other kinds of studies. This new study does both. "We can identify every single relevant beneficial mutation," said Nguyen Ba, citing new technology that allowed the research team to follow specific genomes (or lineages) for approximately a thousand generations. Cvijović, formerly a graduate student in Desai's lab and now a researcher at Princeton, said the research could have gone on indefinitely: "A thousand generations is about three months of growth in our conditions. That's enough time to see big changes happening." Such in-depth, long-term research was possible because of a technological advance in the methodology that allowed what Nguyen Ba called the "re-barcoding" of DNA. Using an enzyme to place a marker, the "barcode," at a specific DNA site, the researchers were able to follow the DNA of yeast through multiple generations. By re-tagging and re-barcoding subsequent generations to record their lineage, the team could then observe how this DNA was transmitted, noting what survived, and what thrived -- or came to dominate -- as generations passed. What they discovered included a few surprises. According to the existing theory, the "fittest" DNA would be that which showed up most frequently in subsequent generations. However, the scientists observed "fluctuations" that the theories could not account for. "Mutations and genotypes that seem to have fallen behind can leapfrog and dominate," said Cvijović. What that means, she says, will be the subject of future research. However, it implies that evolution is, indeed, even more complex than previously thought. "Our experiment suggests there may be a wide range of a large number of strongly beneficial mutations," she said. "And their benefits are both very strong and very different from one another." Story Source: Materials provided by Harvard University. Note: Content may be edited for style and length. Journal Reference:
New Model of Heritable Change The common view of heredity is that all information passed down from one generation to the next is stored in an organism's DNA. But Antony Jose, associate professor of cell biology and molecular genetics at the University of Maryland, disagrees. In two new papers, Jose argues that DNA is just the ingredient list, not the set of instructions used to build and maintain a living organism. The instructions, he says, are much more complicated, and they're stored in the molecules that regulate a cell's DNA and other functioning systems. Jose outlined a new theoretical framework for heredity, which was developed through 20 years of research on genetics and epigenetics, in peer-reviewed papers in the Journal of the Royal Society Interface and the journal BioEssays. Both papers were published on April 22, 2020. Jose's argument suggests that scientists may be overlooking important avenues for studying and treating hereditary diseases, and current beliefs about evolution may be overly focused on the role of the genome, which contains all of an organism's DNA. "DNA cannot be seen as the 'blueprint' for life," Jose said. "It is at best an overlapping and potentially scrambled list of ingredients that is used differently by different cells at different times." For example, the gene for eye color exists in every cell of the body, but the process that produces the protein for eye color only occurs during a specific stage of development and only in the cells that constitute the colored portion of the eyes. That information is not stored in the DNA. In addition, scientists are unable to determine the complex shape of an organ such as an eye, or that a creature will have eyes at all, by reading the creature's DNA. These fundamental aspects of anatomy are dictated by something outside of the DNA. Jose argues that these aspects of development, which enable a fertilized egg to grow from a single cell into a complex organism, must be seen as an integral part of heredity. Jose's new framework recasts heredity as a complex, networked information system in which all the regulatory molecules that help the cell to function can constitute a store of hereditary information. Michael Levin, a professor of biology and director of the Tufts Center for Regenerative and Developmental Biology and the Allen Discovery Center at Tufts University, believes Jose's approach could help answer many questions not addressed by the current genome-centric view of biology. Levin was not involved with either of the published papers. "Understanding the transmission, storage and encoding of biological information is a critical goal, not only for basic science but also for transformative advances in regenerative medicine," Levin said. "In these two papers, Antony Jose masterfully applies a computer science approach to provide an overview and a quantitative analysis of possible molecular dynamics that could serve as a medium for heritable information." Jose proposes that instructions not coded in the DNA are contained in the arrangement of the molecules within cells and their interactions with one another. This arrangement of molecules is preserved and passed down from one generation to the next. In his papers, Jose's framework recasts inheritance as the combined effects of three components: entities, sensors and properties. Entities include the genome and all the other molecules within a cell that are needed to build an organism. Entities can change over time, but they are recreated with their original structure, arrangement and interactions at the start of each generation. "That aspect of heredity, that the arrangement of molecules is similar across generations, is deeply underappreciated, and it leads to all sorts of misunderstandings of how heredity works," Jose said. Sensors are specific entities that interact with and respond to other entities or to their environment. Sensors respond to certain properties, such as the arrangement of a molecule, its concentration in the cell or its proximity to another molecule. Together, entities, sensors and properties enable a living organism to sense or 'know' things about itself and its environment. Some of this knowledge is used along with the genome in every generation to build an organism. "This framework is built on years of experimental research in many labs, including ours, on epigenetics and multi-generational gene silencing combined with our growing interest in theoretical biology," Jose said. "Given how two people who contract the same disease do not necessarily show the same symptoms, we really need to understand all the places where two people can be different -- not just their genomes." The folly of maintaining a genome-centric view of heredity, according to Jose, is that scientists may be missing opportunities to combat heritable diseases and to understand the secrets of evolution. In medicine, for instance, research into why hereditary diseases affect individuals differently focuses on genetic differences and on chemical or physical differences in entities. But this new framework suggests researchers should be looking for non-genetic differences in the cells of individuals with hereditary diseases, such as the arrangement of molecules and their interactions. Scientists don't currently have methods to measure some of these things, so this work points to potentially important new avenues for research. In evolution, Jose's framework suggests that organisms could evolve through changes in the arrangement of molecules without changes in their DNA sequence. And in conservation science, this work suggests that attempts to preserve endangered species through DNA banks alone are missing critical information stored in non-DNA molecules. Jose acknowledged that there will be much debate about these ideas, and experiments are needed to test his hypotheses. But, he said, preliminary feedback from scientists like Levin and other colleagues has been positive. "Antony Jose's generalization of memory and encoding via the entity-sensor-property framework sheds novel insights into evolution and biological complexity and suggests important revisions to existing paradigms in genetics, epigenetics and development," Levin said. Story Source: Materials provided by University of Maryland. Note: Content may be edited for style and length. Journal References:
Cite This Page: University of Maryland. "DNA may not be life's instruction book -- just a jumbled list of ingredients: Researcher develops potentially revolutionary framework for heredity and evolution in which inheritable information is stored outside the genome.." ScienceDaily. ScienceDaily, 22 April 2020. <www.sciencedaily.com/releases/2020/04/200422112303.htm>.
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The Nash Eqiilibrium And Coperative Adaptation
In a group of animals, who deals with new information coming from the environment? Researchers have discovered that the answer lies not in who, but in where: information can be processed, not only by individual animals, but also in the invisible connections between them. In a paper published in the Proceedings of the National Academy of Sciences, an international team of scientists provides evidence of information processing occurring in the physical structure of animal groups. The study demonstrates that animals can encode information about their environment in the architecture of their groups and provides rare insight into how animal collectives are able to behaviourally adapt to a changing world.
For behaviour to be of any use, it needs to be modulated according to what's happening in the world around us. We see this in ourselves when we respond to a sudden noise: in a crowded street in broad daylight we might not notice the noise; but in an unfamiliar alley in darkness it might send our hearts racing. This context-dependent modification of behaviour -- known as behavioural plasticity -- has been very well studied in individual animals. What is much less known is how the process occurs in animal groups.
"When we start looking at how groups respond to their environment, it introduces a possibility that does not exist when you look at individual animals," says senior author Iain Couzin who leads the Centre for the Advanced Study of Collective Behaviour at the University of Konstanz, one of the University of Konstanz' Clusters of Excellence, and the Department of Collective Behaviour at the Max Planck Institute of Animal Behavior in Konstanz. "When you form groups, you suddenly have a network system where social interactions exist, and we wondered whether this invisible architecture was in fact contributing to how groups can respond to changes in the environment."
The researchers focused on two possible mechanisms that could contribute to groups' changing responsiveness: 1) changes in the sensitivity of individuals and 2) changes in the connections between them. They examined how groups of juvenile golden shiner fish (Notemigonus crysoleucas) respond to danger in the environment. "Danger is one of the most important things that animals need to respond to if they are to survive," says Couzin. Researchers were able to manipulate groups' perception of danger by introducing a substance called schreckstoff -- a chemical cocktail released from the skin of fish after injury -- into the water. Sensing the chemical, fish perceive the risk of a predator nearby, and thereby display alarm behaviour known as "startle" events.
The researchers found that indeed, groups startled more frequently and many more fish participated in startle events when fish perceived greater risk in the environment. However, they found that the increased startle rates were not because individual fish were more sensitive to sensory cues. Rather, it was the physical structure of the group -- how the individuals are positioned with respect to one another and how far apart they are -- that was the best predictor of a startle event. In other words, by changing the structure of the group, by coming closer together, the strength of the social connectivity among the individuals increased -- allowing them to respond effectively and rapidly to changes in their environment, as a collective.
"Making each individual more sensitive to risk can lead to an excessive number of false alarms propagating through the group," says Couzin. "On the other hand, strengthening social connections allows individuals to amplify information about risk, but buffers against the system becoming overly sensitive."
The researchers believe that the results can lead to important insights into the relationships between structure of social networks and how to effectively process information. Such results could benefit the development of new technologies for efficiently solving problems through collective intelligence, such as networked robots.
Says Couzin: "We have traditionally assumed that intelligence resides in our brains, in the individual animal. But we have found the first evidence that intelligence can also be encoded in the hidden network of communication between us."
Story Source:
Materials provided by University of Konstanz. Note: Content may be edited for style and length.
Journal Reference:
- Matthew M.G. Sosna, Colin R. Twomey, Joseph Bak-Coleman, Winnie Poel, Bryan C. Daniels, Pawel Romanczuk and Iain D. Couzin. Individual and collective encoding of risk in animal groups. PNAS, 2019
Cite This Page: University of Konstanz. "Uncovering hidden intelligence of collectives." ScienceDaily. ScienceDaily, 23 September 2019. <www.sciencedaily.com/releases/2019/09/190923155130.htm>. edit.
SUBJECTIVE AWARENESS AND THE NASH EQUILIBRIUM
Genetics isn't as important as once thought for the evolution of altruistic social behavior in some organisms, a new insight into a decade-long debate.
This is the first empirical evidence that suggests social behavior in eusocial species -- organisms that are highly organized, with divisions of infertile workers -- is only mildly attributed to how related these organisms are to each other.
In evolutionary biology, fitness refers to an organism's reproductive success and propagation of its genes. When researchers at Hokkaido University studied the foraging and nesting behaviors of the eusocial species Lasioglossum baleicum, commonly known as the sweat bee, they found that the fitness was more a result of the bees' cooperative behaviour than it was a result of their genetic similarity.
This evidence is contrary to earlier theories that attributed altruistic selfless behavior in eusocial species to genetic relatedness and a want to ensure the propagation of their genes. In some insect species, genetic similarity is higher between sisters than between a sister and its own offspring, and this has been considered the key driver to the formation of a eusociety.
Evolutionary biologist Eisuke Hasegawa and his colleagues studied five aggregations of sweat bee nests in various areas on the island of Hokkaido in Japan. In each aggregation, there were two types of nests: those in which multiple females worked together to take care of the offspring of a single queen, and those in which a mother bee took care of her offspring on her own.
Queen bees lay several eggs at a time. They hatch as predominantly infertile females, who grow to become workers. The team marked all the adult bees in the nests so they could identify them, then studied how often and for how long each adult female left the nest to forage over a 12-hour period.
They found that the females working in the cooperative nests foraged more often than the females from the solitary nests. In addition, solitary nests were devoid of adult females much more often than social nests, leaving the nests more vulnerable to predators.
Ants are the main predator of sweat bees. A female sweat bee protects the offspring in her nest from scout ants, which can recruit many other ants to attack, by plugging the nest opening with her head. This is why solitary adult females can only leave their nests for short periods of time. Cooperative nests, on the other hand, are more efficiently defended.
Individual females in social nests are known to have higher fitness than solitary females, meaning that social bees are more successful in propagating their genes. The team has found that 92% of the increase in fitness can be attributed to the benefit of grouping -- efficient foraging and defense -- while the rest is due to the genetic similarity between the individuals.
The findings indicate that, contrary to previous theories, the main contributing aspect of fitness in a social nest comes from the benefit of grouping. "There has been a decade-long debate among scientists as to whether genetic similarity or the benefit of grouping is the primary drive of sociality. Our study could help reveal some of the factors behind the evolution of cooperation, including among humans, by quantifying how much cooperative behavior contributes to the increased fitness of altruistic individuals in a group," says Hasegawa.
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Materials provided by Hokkaido University. Note: Content may be edited for style and length.
Journal Reference:
- Yusaku Ohkubo, Tatsuhiro Yamamoto, Natsuki Ogusu, Saori Watanabe, Yuuka Murakami, Norihiro Yagi, Eisuke Hasegawa. The benefits of grouping as a main driver of social evolution in a halictine bee. Science Advances, 2018; 4 (10): e1700741 DOI: 10.1126/sciadv.1700741
CRYPTIC VARIATION
Journal Reference:- Jia Zheng, Joshua L. Payne, Andreas Wagner. Cryptic genetic variation accelerates evolution by opening access to diverse adaptive peaks. Science, 2019; 365 (6451): 347 DOI: 10.1126/science.aax1837
Laboratory populations that quietly amass 'cryptic' genetic variants are capable of surprising evolutionary leaps, according to a paper in the July 26 issue of Science. A better understanding of cryptic variation may improve directed evolution techniques for developing new biomolecules for medical and other applications. Genetic variation -- that is, accumulated mutations in the DNA -- is the fuel for all evolutionary change: the more genetic variation, the faster evolution works and the more possibilities for novel adaptive solutions. But one kind of genetic variation -- hidden, or "cryptic," variation -- doesn't alter the appearance or behavior of an organism in its usual environment. "It's an underappreciated kind of genetic variation," says corresponding author Andreas Wagner, an evolutionary biologist at the University of Zurich and external professor at the Santa Fe Institute, "and it plays an important role in evolution." Previous work has shown that cryptic variation in natural populations promotes rapid evolutionary adaptation. But the underlying molecular mechanisms were unclear. To explore those mechanisms, Wagner's team worked with populations of the gut bacterium E. coli that carried a plasmid with a gene for a yellow fluorescent protein (YFP). The team designed a two-stage experiment. In stage 1, they used mutagenic PCR to increase variation in the YFP gene. Simultaneously, they selected for a narrow range of yellow fluorescence. Any bacteria not sufficiently yellow were excluded, a process called 'stabilizing selection.' In this way, they built up deep stores of cryptic genetic variation without altering the yellow color of the YFP protein. During stage 2, the team changed the selection rules and began selecting for E. coli that fluoresced in the green part of the spectrum ('directional selection'). They also introduced control populations of E. coli that lacked enhanced cryptic variation in YFP. The E. coli cell lines with stores of cryptic variation evolved green fluorescent protein (from YFP genes) that were both greener and genetically more diverse than any produced by the control E. coli lineages. In the experiment, says co-author Joshua Payne (ETH Zurich), cryptic variation did more than drive evolutionary adaptation faster. Cell lines with deep reserves of cryptic variation evolved greener YFP proteins, forms of the protein that were inaccessible to regular bacteria, and they evolved by multiple unique routes not available to regular E. coli. Current laboratory directed evolution often leads to the same evolutionary outcomes each time. The new work shows how amassing cryptic variation can open doors to otherwise inaccessible regions of protein sequence space, says first author Jia Zheng, a postdoctoral researcher at the University of Zurich. In the wild, cryptic variation helps fish adapt to life in caves. In the lab, cryptic variation might help a biomolecule bind a new receptor. "Our work can help develop new directed evolution strategies to find innovative biomolecules for biotechnological and medical applications," says Zheng. Like a fat savings account, cryptic variation is a store of variation that becomes available in an emergency to fuel rapid evolutionary change critical to the survival of a lineage and useful for molecular biologists.
Story Source: Materials provided by Santa Fe Institute. Note: Content may be edited for style and length.
Journal Reference: Jia Zheng, Joshua L. Payne, Andreas Wagner. Cryptic genetic variation accelerates evolution by opening access to diverse adaptive peaks. Science, 2019; 365 (6451): 347 DOI: 10.1126/science.aax1837
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THE NASH EQUILIBRIUM of SELF INTEREST/SHARED INTEREST
William Blake may have seen a world in a grain of sand, but for scientists at MIT the smallest of all photosynthetic bacteria holds clues to the evolution of entire ecosystems, and perhaps even the whole biosphere.
The key is a tiny bacterium called Prochlorococcus, which is the most abundant photosynthetic life form in the oceans. New research shows that this diminutive creature's metabolism has evolved in a way that may have helped trigger the rise of other organisms, to form a more complex marine ecosystem. Its evolution may even have helped to drive global changes that made possible the development of Earth's more complex organisms.
The research also suggests that the co-evolution of Prochlorococcus and its interdependent co-organisms can be seen as a microcosm of the metabolic processes that take place inside the cells of much more complex organisms.
The new analysis is published this week in the journal Proceedings of the National Academy of Sciences, in a paper by postdoc Rogier Braakman, Professor Michael Follows, and Institute Professor Sallie (Penny) Chisholm, who was part of the team that discovered this tiny organism and its outsized influence.
"We have all these different strains that have been isolated from all over the world's oceans, that have different genomes and different genetic capacity, but they're all one species by traditional measures," Chisholm explains. "So there's this extraordinary genetic diversity within this single species that allows it to dominate such vast swaths of Earth's oceans."
Because Prochlorococcus is both so abundant and so well-studied, Braakman says it was an ideal subject for trying to figure out "within all this diversity, how do the metabolic networks change? What drives that, and what are the consequences of that?"
They found a great amount of variation in the bacteria's "metabolic network," which refers to the ways that materials and energy pass in and out of the organism, along its phylogeny. The fact that such significant changes have taken place over the course of Prochlorococcus evolution "tells you something quite dramatic," he says, because these metabolic processes are so fundamental to the organism's survival that "it's like the engine of the system. So imagine trying to change the engine of your car while you're driving. It's not easily done, so if something is changing, it's telling you something significant."
The variations form a kind of layered structure, with more ancestral variants living deeper in the water column and more recent variants living near the surface. The team found that as Prochlorococcus started out living in the top layers of the ocean, where light is abundant but food is relatively scarce, it developed a higher and higher rate of metabolism. It took in more solar energy and used that to power a stronger uptake of scarce nutrients from the water -- in effect, creating a more powerful vacuum cleaner but in the process also generating more waste, Braakman says.
As newer variants vacuumed up nutrients in the surface layers, more ancestral types had to move down to greater depths where nutrients levels remained higher, ultimately resulting in the layered structure seen today.
The carbon compounds that make up Prochlorococcus' waste in turn provided nutrients that drove the evolution of another kind of bacteria, known as SAR11, whose own waste products were useful to Prochlorococcus, thus forming a cooperative system that benefited both organisms. The mutual recycling of waste reinforces the collective maximization of metabolic rate. "It looks like the system is in fact evolving to maximize the total throughput" of energy, not just that of individual organisms, Braakman says.
"As they optimize their ability to acquire nutrients, cells produce more organic carbon and end up promoting greater levels of mutualism," Follows adds.
That interdependent, cooperative relationship is very similar to the relationship between mitochondria and chloroplasts, the two kinds of subunits that provide the energy inside the cells of all forms of plant life, Braakman says. Chloroplasts collect energy from sunlight and use it to form chemical compounds that transfer energy to mitochondria, which can in turn release and transfer carbon and energy back to chloroplasts and the rest of the cell -- through pathways very similar to those used by Prochlorococcus and SAR11.
Other features of the two systems are also very similar, including their photosynthetic pigments and how they deal with the detoxification of hydrogen peroxide. This suggests parallel evolutionary processes produced the same outcome in very different environments. "Plant cells really look like microscopic ocean microbial ecosystems," he explains.
Partly because of those parallels, Braakman says this dynamic could potentially describe the evolution of the biosphere more generally. He suggests that the mathematical descriptions of Prochlorococcus evolution, which he and Follows developed together, emerge from basic principles of kinetics and thermodynamics and so could provide some insights into other systems as well. "It could be a universal kind of dynamic," he says.
"This framework can also help us model the interactions of life, sunlight, and ocean chemistry at the ocean scale," Follows says.
The metabolic evolution of Prochlorococcus may have had one other important effect: Through a complex geochemical cycle involving the carbon compounds the microbe produced and their interactions with iron, the bacteria may have contributed to a significant rise in oxygen in Earth's atmosphere around half a billion years ago, from very low levels up to near-modern levels. This major rise in oxygen is believed to have unleashed a rapid explosion of new species also known as the Cambrian explosion, which saw the birth of most major animal phyla.
What this analysis suggests, he says, "is what looks like a directional evolutionary process, which is steadily marching toward a direction where it's increasing the energy flux through the system. One of the consequences of that is that then oxygen ended up rising in the atmosphere, and the complexity of the ecosystem increased."
A lot of evolutionary theory emphasizes competition, Braakman says, where "there are limited resources and we're all fighting for them. But what this evolutionary dynamic is saying is that it's a way of increasing the resources for the whole system, so everyone is better off. It increases total system resources."
This work, Chisholm says, demonstrates that "you really have to think about evolution at all these scales, to understand it. It's not just about a bunch of selfish genes jumping around. If you want to understand life in all its dimensions, you have to look at the genes, but also all the way up to the ecosystems. None of it will make sense if you don't look at it at all those scales."
UBUNTU...I am because we are!
Story Source:
Materials provided by Massachusetts Institute of Technology. Original written by David L. Chandler. Note: Content may be edited for style and length.
Journal Reference:
Rogier Braakman, Michael J. Follows, Sallie W. Chisholm. Metabolic evolution and the self-organization of ecosystems. Proceedings of the National Academy of Sciences, 2017; 201619573 DOI: 10.1073/pnas.1619573114
THE NASH EQUILIBRIUM WITHIN AND AMONG SPECIES
Biologists at UC San Diego who recently found that bacteria resolve social conflicts within their communities and communicate with one another like neurons in the brain have discovered another human-like trait in these apparently not-so-simple, single-celled creatures.
Bacteria living in diverse communities called "biofilms" create what are essentially electronic advertisements, the scientists report in a paper published in this week's issue of the journal Cell, by sending long-range electrical signals to other bacterial species that can lead to the recruitment of new members to their biofilm community.
"We've discovered that bacterial biofilm communities can actively modulate the motile behavior of diverse bacterial species through electrical signals," said Gürol Süel, a professor of molecular biology, Associate Director of the San Diego Center for Systems Biology and Howard Hughes Medical Institute -- Simons Faculty Scholar at UC San Diego, who headed the research effort. "In this way, bacteria within biofilms can exert long-range and dynamic control over the behavior of distant cells that are not part of their communities."
Biofilms are communities of bacteria and other microorganisms that form thin structures on surfaces -- such as the tartar that develops on teeth -- that are highly resistant to chemicals and antibiotics. Because not much is known about how they form, recruit other microorganisms and resist attack, such information about their behavior has practical applications -- from preventing tartar formation on teeth to avoiding Staph infections in hospitals.
But the idea that bacteria ensconced in their protective biofilm villages behave like sophisticated marketing agents -- advertising the presence of their communities by sending out electronic messages -- overturns fundamental beliefs that both scientists and the general public have about these supposedly lowly creatures.
"Our study shows that bacteria living in biofilm communities do something similar to sending electronic messages to friends," said Jacqueline Humphries, a doctoral student working in Süel's laboratory and the first author of the paper. "In fact, the mechanism we discovered is general. We found that bacteria from one species can send long-range electrical signals that will lead to the recruitment of new members from another species. As a result, we've identified a new mechanism and paradigm for inter-species signaling."
The UC San Diego biologists discovered in their laboratory work, which integrated experiments with mathematical modeling, that a biofilm composed of a single species of Bacillus subtilis bacteria was able to recruit bacteria of a different species -- in this case, Pseudomonas aeruginosa -- through electrical signaling.
Using microfluidic growth chambers, the biologists documented the process by which potassium ion electrical signaling generated by B. subtilis biofilms attracted distant cells within the chambers to the edge of electrically oscillating biofilms.
Süel and his team of graduate students and postdoctoral fellows discovered in the summer of 2015 that oscillations within biofilm communities resolved a social conflict between individual cells that were cooperating, but also had to compete for food.
Bacteria at the outer edge of the biofilm are closest to nutrients necessary for growth and could starve the sheltered interior cells. But the scientists discovered that oscillating biofilms develop what they call "metabolic codependence" by putting the brakes periodically on the outer cells' growth to give the interior cells access to nutrients.
Not long after, Süel and his team discovered that bacteria living in biofilm communities communicate with one another electronically through proteins called "ion channels," an electrical signaling method similar to that used by neurons in the human brain.
Their most recent discovery -- that bacteria in biofilms can recruit other species with long-range electrical signals -- could turn out to be not only the most surprising of the team's findings, but perhaps the most significant for our understanding of how bacteria impact human health.
"Our latest discovery suggests that the composition of mixed species bacterial communities, such as our gut microbiome, could be regulated through electrical signaling," said Süel. "It may even be possible that bacterial and human gut cells can interact electrically within the human gut. Our work may in the future even lead to new electrical-based biomedical approaches to control bacterial behavior and communities."
Other co-authors of the paper were biologists Jintao Liu and Arthur Prindle, postdoctoral researchers in Süel's laboratory; biologist Fang Yuan, a doctoral student in the lab; UC San Diego physicist Liyang Xiong; Heidi Arjes of Stanford University and Lev Tsimring, a research scientist and associate director of UC San Diego's Biocircuits Institute.
Genomic Plasticity and Genetic Transfer
The evolutionary pressure to pass on DNA can produce behavior that otherwise makes no sense in a struggle to survive. Rams bash heads in fights over females; peacocks grow elaborate tail feathers that attract mates and predators alike. Sexual selection can sometimes explain phenomena that natural selection alone cannot. But could bacteria exhibit sexual selection? In an Opinion article published September 4 in the journal Trends in Microbiology, researchers at the University of Exeter argue that some bacteria might.
Bacteria usually clone themselves to reproduce, but they are also known to swap DNA. A donor bacteria cell can transfer genes to a recipient cell in a process called lateral gene transfer, which can happen through three mechanisms: transduction, conjugation, and transformation. The research group thinks this DNA exchange (and transformation in particular) could be governed by sexual selection at times.
"Transformation and other forms of DNA transfer are very prevalent in almost all types of bacteria and have a huge effect on their evolution. For instance, bacteria can take up antibiotic resistance genes from other strains and species, with profound consequences for human health," says first author Michiel Vos, a microbiologist at the University of Exeter. "So, it is important to try to understand exactly why they have evolved to release and take up DNA."
In transformation, a donor cell releases its DNA into the surrounding environment either by actively pumping it out of the cell or by simply rupturing and spilling its contents. The recipient cell might then take up the free-floating DNA and incorporate it into its own genome. When the recipient cell later clones itself, it propagates a genome that is mostly self-DNA but has snippets of donor DNA.
Scientists have several theories explaining why bacteria do this. Some focus on natural selection and how new donor DNA benefits cell survival. Others argue that transformation isn't about natural selection at all but other functions, such as using DNA from the environment as food or for repair, and that the genetic mixing is just a coincidental byproduct. Vos and his colleagues think that although natural selection must act on DNA release and uptake, there could be additional benefits of sexual selection.
"One analogy we drew, which will be controversial to some, is between DNA release and uptake as, respectively, the male and female functions," says Vos. "Female and male functions are defined by the size of gametes -- large eggs or small sperm -- and, of course, bacteria do not have gametes."
But Vos and his colleagues see several testable analogies between transformation in bacteria and sexual selection in other organisms. For example, bacteria invest energy into DNA release, and male animals invest energy into creating lots of sperm -- ditto for costly DNA uptake and reproduction and investing energy to create an egg cell, of which only half of the genetic material derives from the mother. Future studies could examine how much energy different bacteria species invest in transformation, which bacteria pass on more of their DNA, and what gave those bacteria an advantage.
Sexual selection can sometimes result in coercion where (usually) males evolve offensive tactics to coerce females into mating. This in turn selects for females to become resistant to the coercion. In bacteria, coercion could take the form of releasing chemical signals that prime other bacteria to take up DNA. In another possible example of sexual selection, recent research has found that some bacterial species take up DNA after selectively lysing (rupturing) unrelated strains, which can be expected to increase the chances of taking up novel adaptive genes from the ruptured cells.
"We believe sex by coercion might happen in bacteria too," says Vos. The Exeter scientists are now planning experiments to test these ideas.
In the roughly two dozen species of bacteria that serve as model systems for transformation, there is great variation in the genetic mechanisms and ecological cues controlling DNA uptake and release. It is likely that this diversity is much greater in the millions of bacterial species that have yet to be described. The authors hope that future research on bacterial gene exchange will take into account sexual-selection theory developed in the context of animals.
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Materials provided by Cell Press. Note: Content may be edited for style and length.
Journal Reference:
Cite This Page: Cell Press. "The argument for sexual selection in bacteria." ScienceDaily. ScienceDaily, 4 September 2019. <www.sciencedaily.com/releases/2019/09/190904113220.htm>.
The evolutionary pressure to pass on DNA can produce behavior that otherwise makes no sense in a struggle to survive. Rams bash heads in fights over females; peacocks grow elaborate tail feathers that attract mates and predators alike. Sexual selection can sometimes explain phenomena that natural selection alone cannot. But could bacteria exhibit sexual selection? In an Opinion article published September 4 in the journal Trends in Microbiology, researchers at the University of Exeter argue that some bacteria might.
Bacteria usually clone themselves to reproduce, but they are also known to swap DNA. A donor bacteria cell can transfer genes to a recipient cell in a process called lateral gene transfer, which can happen through three mechanisms: transduction, conjugation, and transformation. The research group thinks this DNA exchange (and transformation in particular) could be governed by sexual selection at times.
"Transformation and other forms of DNA transfer are very prevalent in almost all types of bacteria and have a huge effect on their evolution. For instance, bacteria can take up antibiotic resistance genes from other strains and species, with profound consequences for human health," says first author Michiel Vos, a microbiologist at the University of Exeter. "So, it is important to try to understand exactly why they have evolved to release and take up DNA."
In transformation, a donor cell releases its DNA into the surrounding environment either by actively pumping it out of the cell or by simply rupturing and spilling its contents. The recipient cell might then take up the free-floating DNA and incorporate it into its own genome. When the recipient cell later clones itself, it propagates a genome that is mostly self-DNA but has snippets of donor DNA.
Scientists have several theories explaining why bacteria do this. Some focus on natural selection and how new donor DNA benefits cell survival. Others argue that transformation isn't about natural selection at all but other functions, such as using DNA from the environment as food or for repair, and that the genetic mixing is just a coincidental byproduct. Vos and his colleagues think that although natural selection must act on DNA release and uptake, there could be additional benefits of sexual selection.
"One analogy we drew, which will be controversial to some, is between DNA release and uptake as, respectively, the male and female functions," says Vos. "Female and male functions are defined by the size of gametes -- large eggs or small sperm -- and, of course, bacteria do not have gametes."
But Vos and his colleagues see several testable analogies between transformation in bacteria and sexual selection in other organisms. For example, bacteria invest energy into DNA release, and male animals invest energy into creating lots of sperm -- ditto for costly DNA uptake and reproduction and investing energy to create an egg cell, of which only half of the genetic material derives from the mother. Future studies could examine how much energy different bacteria species invest in transformation, which bacteria pass on more of their DNA, and what gave those bacteria an advantage.
Sexual selection can sometimes result in coercion where (usually) males evolve offensive tactics to coerce females into mating. This in turn selects for females to become resistant to the coercion. In bacteria, coercion could take the form of releasing chemical signals that prime other bacteria to take up DNA. In another possible example of sexual selection, recent research has found that some bacterial species take up DNA after selectively lysing (rupturing) unrelated strains, which can be expected to increase the chances of taking up novel adaptive genes from the ruptured cells.
"We believe sex by coercion might happen in bacteria too," says Vos. The Exeter scientists are now planning experiments to test these ideas.
In the roughly two dozen species of bacteria that serve as model systems for transformation, there is great variation in the genetic mechanisms and ecological cues controlling DNA uptake and release. It is likely that this diversity is much greater in the millions of bacterial species that have yet to be described. The authors hope that future research on bacterial gene exchange will take into account sexual-selection theory developed in the context of animals.
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Materials provided by Cell Press. Note: Content may be edited for style and length.
Journal Reference:
- Vos et al. Sexual selection in bacteria? Trends in Microbiology, 2019 DOI: 10.1016/j.tim.2019.07.009
Cite This Page: Cell Press. "The argument for sexual selection in bacteria." ScienceDaily. ScienceDaily, 4 September 2019. <www.sciencedaily.com/releases/2019/09/190904113220.htm>.
GENOMIC PLASTICITY CREATING DIFFERENT SPECIATION RATES
Evolution is actually a Sadie Hawkins dance, as new research shows females not only determine whether male animals develop bright colors, but also how fast new species develop.
Research led by David Reznick, a UC Riverside biology professor, used fish often seen in pet stores, like guppies and swordtails, to test a hypothesis proposed by David and Jean Zeh at the University of Nevada, Reno. They predicted that the way mothers nurture their young influences the evolution of male traits, and Reznick's team is the first to find that the prediction was correct.
A paper describing the research was published online today in Nature Communications.
Reznick was inspired to test the hypothesis while wandering the aisles of a pet store. Having spent more than a decade studying fish in the guppy family, he knew the ones in the store had a few things in common.
"The fish I saw that day all belong to the Poeciliidae family, which give birth to live young, rather than lay eggs. Some of them even have placentas, like mammals," Reznick said. "The ones offered for sale were only species with colorful males and all of those species had mothers that lack placentas. I wanted to know how having this type of mother might relate to the evolution of male traits."
To answer his question, the team constructed a family tree using the DNA from more than 170 species in the Poeciliidae family of freshwater fish. They then mapped male and female traits on to the tree, reconstructing how male and female traits evolved throughout the fish family.
For the fish without placentas, choosing a mate can be higher stakes.
"When mothers lack a placenta, they've already invested all they've got to give into the eggs prior to fertilization," Reznick said. "So, the mothers are picky about the males they choose."
In fish where the mothers do have a placenta, it's a different game. In these species the eggs are smaller, and the mother hasn't invested a lot in them yet. A mother with a placenta has the ability to choose the father after mating, by influencing which sperm fertilize the eggs or possibly by aborting eggs she doesn't want.
Analyzing the DNA tree of the fish family, the team found that the branches of the family tree with mothers who lack placentas are also those that give rise to the flashier males.
The team then investigated a second prediction by David and Jean Zeh: that animals with placentas would diverge faster from one species into two. Here, Reznick's team proved this prediction wrong.
Fish species with fancy males formed new species twice as fast as those with plain males. What this means is that in these fish, there is a connection between the way mothers nurture offspring, how they choose mates, and how fast their kind is destined to multiply into a new species.
Members of the international research team included Andrew Furness of the University of Hull in the U.K., Bart Pollux of Wageningen University in the Netherlands, Robert Meredith of Montclair State University in New Jersey, as well as UC Riverside's Mark Springer.
Though this analysis was performed using fish, Reznick says the underlying principles are broadly applicable throughout the animal kingdom. Many animals have evolved the ability to produce live young and many of these have evolved something like a placenta. He expects that the same connections between evolution of male and female traits and speciation rate are waiting to be discovered.
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Materials provided by University of California - Riverside. Note: Content may be edited for style and length.
Journal Reference:
- Andrew I. Furness, Bart J. A. Pollux, Robert W. Meredith, Mark S. Springer, David N. Reznick. How conflict shapes evolution in poeciliid fishes. Nature Communications, 2019; 10 (1) DOI: 10.1038/s41467-019-11307-5
GENOMIC PLASTICITY
(Genes for New Species Created by Species That Don't Use Them)
In a new study, published in Nature, an international research group led from Uppsala University in Sweden presents the discovery of a group of microbes that provide new insights as to how complex cellular life emerged. The study provides new details of how, billions of years ago, complex cell types that comprise plants, fungi, but also animals and humans, gradually evolved from simpler microbial ancestors.
Life on our planet can be divided into three major groups. Two of these groups are represented by tiny microbes, the Bacteria and the Archaea. The third group of organisms comprises all visible life, such as humans, animals, and fungi -- collectively known as eukaryotes. Whereas the cells of bacteria and archaea are generally small and simple, eukaryotes are made up of large and complex cell types. The origin of these complex cell types has long been a mystery to the scientific community, but now an international collective of researchers led by Uppsala University has identified a group of microorganisms that provides a unique insight into the evolutionary transition from simple to complex cells.
Based on pioneering work from the acclaimed biologist Carl Woese, it has been known that eukaryotes at some point shared a common ancestor with archaea. It was also clear that symbiosis -- a process involving an intimate collaboration between two cell types -- played an important role in this process. Most scientists share the view that a symbiosis in which an archaeal host cell took up a bacterium ultimately gave rise to eukaryotes. Yet, whether this symbiosis was the cause or rather the consequence of the evolution of complex cells remained an open question.
In this weeks' edition of Nature, researchers from Uppsala University in Sweden, along with collaborators from the USA, Japan, Denmark and New Zealand report the discovery of a new group of Archaea, the Asgard archaea, which reveal important details on how eukaryotic cells evolved their complexity.
"The evolution of complex cell types has been a long and complicated process that is poorly understood. By using new methods to obtain genome data from microbes that cannot be grown in the laboratory, we identified a new archaeal group that is related to the host cell from which eukaryotic cells evolved. These are very exciting times," says Thijs Ettema at the Department of Cell and Molecular Biology, Uppsala University, who lead the scientific team that carried out the study.
In 2015, Thijs Ettema and colleagues published a breakthrough study in which genomic data was described of 'Loki', an archaeon living in the ocean floor that represented the closest living micro-organism of complex cellular life. In the current study, which corroborates these previous findings, several new Loki-related archaea are described.
"These organisms are our closest microbial relatives, and we know next to nothing about them. Current methods allow us to take a first genetic sneak peek. It is really exciting!'' says Thijs Ettema.
"Our findings are based on analysis of genetic material that was directly obtained from the environment. We have actually never seen these cells," says Jimmy Saw, researcher at the Department of Cell and Molecular Biology, Uppsala University, and co-lead author of the paper.
"We named these new archaea Thor, Odin and Heimdall after the Norse gods, and together with Loki, they form the Asgard archaea. Interestingly, these new groups are found in various environments all over the world, and not only in the deep sea, as Loki. So far they are most abundant in sediments," says Eva Fernandez-Caceres, co-lead author from Uppsala University.
The study provides strong evidence that eukaryotes evolved from a lineage that was related to these Asgard archaea.
"Asgard archaea form a well-supported group with the eukaryotes in the tree of life. This indicates that they share a common ancestry," says Kasia Zaremba-Niedzwiedzka, another co-lead author involved in the study from Uppsala University. "This part of the study was rather complicated, and we would clearly benefit from having more data. This is not the end of the story, rather the opposite!"
But the main surprise was found when Asgard genomes were analyzed in more detail.
"We found that Asgard archaea share many genes uniquely with eukaryotes, including several genes that are involved in the formation of structures that give eukaryotic cells their complex character. Such genes had thus far only been found in eukaryotes, indicating that these archaea were somehow primed to become complex. However, the picture is far from being clear on exactly how this could have happened," says Anja Spang, researcher at the Department of Cell and Molecular Biology, Uppsala University.
Studying Asgard archaea in more detail represents a prioritized goal for Thijs Ettema and his research group. The present study shows that these archaea can be found in many more environments, and not just in the ocean floor as thought before. This makes this goal much more tractable.
"It would be great if we could isolate or grow Asgard cells, and study them under the microscope. I am convinced that this will reveal more important clues about how complex cells evolved. Ultimately our microbial ancestry will be uncovered," concludes Thijs Ettema.
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Materials provided by Uppsala University. Note: Content may be edited for style and length.
Journal Reference:
Katarzyna Zaremba-Niedzwiedzka, Eva F. Caceres, Jimmy H. Saw, Disa Bäckström, Lina Juzokaite, Emmelien Vancaester, Kiley W. Seitz, Karthik Anantharaman, Piotr Starnawski, Kasper U. Kjeldsen, Matthew B. Stott, Takuro Nunoura, Jillian F. Banfield, Andreas Schramm, Brett J. Baker, Anja Spang, Thijs J. G. Ettema. Asgard archaea illuminate the origin of eukaryotic cellular complexity. Nature, 2017; DOI: 10.1038/nature21031
EPIGINETC CHANGES THROUGH SUBJECTIVE EXPERIENCES OF CULTURE
A UC San Francisco-led study has identified signatures of ethnicity in the genome that appear to reflect an ethnic group's shared culture and environment, rather than their common genetic ancestry.
The study examined DNA methylation -- an "annotation" of DNA that alters gene expression without changing the genomic sequence itself -- in a group of diverse Latino children. Methylation is one type of "epigenetic mark" that previous research has shown can be either inherited or altered by life experience. The researchers identified several hundred differences in methylation associated with either Mexican or Puerto Rican ethnicity, but discovered that only three-quarters of the epigenetic difference between the two ethnic subgroups could be accounted for by differences in the children's genetic ancestry. The rest of the epigenetic differences, the authors suggest, may reflect a biological stamp made by the different experiences, practices, and environmental exposures distinct to the two ethnic subgroups.
The discovery could help scientists understand how social, cultural, and environmental factors interact with genetics to create differences in health outcomes between different ethnic populations, the authors say, and provides a counterpoint to long-standing efforts in the biomedical research community to replace imprecise racial and ethnic categorization with genetic tests to determine ancestry.
"These data suggest that the interplay between race and ethnicity as social constructs and genetic ancestry as a biological construct is more complex than we had realized," said Noah Zaitlen, PhD, a UCSF assistant professor of medicine and co-senior author on the new study. "In a medical context both elements may provide valuable information."
The research -- published January 3, 2017 in the online journal eLife -- was led by Joshua Galanter, MD, MAS, formerly an assistant professor of medicine, of bioengineering and therapeutic sciences, and of epidemiology and biostatistics at UCSF, who is now a scientist at Genentech. The research was jointly supervised by Zaitlen and co-senior author Esteban Burchard, MD, MPH, a professor of bioengineering and therapeutic sciences and of medicine in UCSF's schools of Pharmacy and Medicine and the Harry Wm. and Diana V. Hind Distinguished Professorship in Pharmaceutical Sciences II at UCSF.
"This is a big advancement of our understanding of race and ethnicity," Burchard said. "There's this whole debate about whether race is fundamentally genetic or is just a social construct. To our knowledge this is the first time anyone has attempted to quantify the molecular signature of the non-genetic components of race and ethnicity. It demonstrates in a whole new way that race combines both genetics and environment."
Teasing apart roles of genetics, environment in ethnic differences in disease
Researchers and clinicians have known for many years that different racial and ethnic populations get diseases at different rates, respond differently to medications, and show very different results on standard clinical tests: "For a whole range of medical tests, whether your physician is told that your lab result is normal or abnormal depends entirely on the race/ethnicity box that you tick on an intake form," Zaitlen said.
It's tempting to assume that such health disparities between races and ethnicities all stem from inherited genetic differences, but that's not necessarily the case. Different racial and ethnic groups also eat different diets, live in neighborhoods with more or less pollution, experience different levels of poverty, and are more or less likely to smoke tobacco, all of which could also impact their health outcomes.
"A lot of our research involves trying to tease apart how much of health differences between populations are genetic and how much are environmental," Zaitlen said.
The researchers turned to epigenetics to search for answers to these questions because these molecular annotations of the genetic code have a unique position between genetic ancestry and environmental influence. Unlike the rest of the genome, which is only inherited from an individual's parents (with random mutations here and there), methylation and other epigenetic annotations can be modified based on experience. These modifications influence when and where particular genes are expressed and appear to have significant impacts on disease risk, suggesting explanations for how environmental factors such as maternal smoking during pregnancy can influence a child's risk of later health problems.
Epigenetic signatures of ethnicity could be biomarkers for shared cultural experiences
In the new study, the team examined methylation signatures in 573 children of self-identified Mexican or Puerto-Rican identity drawn from the GALA II study, a cohort previously developed by Burchard to study environmental and genetic components of asthma risk in Latino children. They identified 916 methylation sites that varied with ethnic identity, but found that only 520 of these differences could be completely explained by genetic ancestry -- 109 could be partially explained by ancestry, while 205 could not be explained by ancestry at all.
Overall, the researchers found that about 76 percent of the effect of ethnicity on DNA methylation could be accounted for by controlling for genetic ancestry, suggesting that nearly a quarter of the effect must be due to other, unknown factors. The researchers found that many of these additional methylation sites corresponded to sites that previous studies had shown to be sensitive to environmental and social factors such as maternal smoking, exposure to diesel exhaust, and psychosocial stress. This led the team to hypothesize that a large fraction of their newly disovered epigenetic markers of ethnicity likely reflect biological signatures of environmental, social, or cultural differences between ethnic subgroups.
"This suggests that using epigenetics as a biomarker could give you a lot of information about environmental exposures within particular populations that's not captured by genetics," Zaitlen said. "Our next step will be to understand how specific epigenetic signatures are linked to particular environmental exposures, and use those signals to understand patient risk."
Scientists and clinicians have increasingly tried to move away from simplistic racial and ethnic categories in disease research, the authors say, and -- with the rise of precision medicine -- in clinical diagnosis and treatment as well. Studies by the Burchard group and others have found that using genetic ancestry rather than ethnic self-identification significantly improves diagnostic accuracy for certain diseases.
But the new data showing that a large fraction of epigenetic signatures of ethnicity reflect something other than ancestry suggests that abandoning the idea of race and ethnicity altogether could sacrifice a lot of valuable information about the drivers of differences in health and disease between different communities.
"Like a standard family history, ethnicity is association with disease for both genetic and environmental reasons," Zaitlen said. "If your dad or mom had a heart attack, that tells doctors a lot about your risk for a heart attack. Part of that is genetic, but part of it is that your lifestyle is influenced heavily by your parents' lifestyle. Your ethnic group is like a much bigger family -- it's partly a matter of genetics, but it also reflects the environment of your broader community."
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Materials provided by University of California - San Francisco. Note: Content may be edited for style and length.
Journal Reference:
Joshua M Galanter, Christopher R Gignoux, Sam S Oh, Dara Torgerson, Maria Pino-Yanes, Neeta Thakur, Celeste Eng, Donglei Hu, Scott Huntsman, Harold J Farber, Pedro C Avila, Emerita Brigino-Buenaventura, Michael A LeNoir, Kelly Meade, Denise Serebrisky, William Rodríguez-Cintrón, Rajesh Kumar, Jose R Rodríguez-Santana, Max A Seibold, Luisa N Borrell, Esteban G Burchard, Noah Zaitlen. Differential methylation between ethnic sub-groups reflects the effect of genetic ancestry and environmental exposures. eLife, 2017; 6 DOI: 10.7554/eLife.20532
HORIZONTAL GENETIC TRANSFER
Some parasitic plants steal genetic material from their host plants and use the stolen genes to more effectively siphon off the host's nutrients. A new study led by researchers at Penn State and Virginia Tech reveals that the parasitic plant dodder has stolen a large amount of genetic material from its hosts, including over 100 functional genes. These stolen genes contribute to dodder's ability to latch onto and steal nutrients from the host and even to send genetic weapons back into the host. The new study appears July 22, 2019, in the journal Nature Plants.
"Horizontal gene transfer, the movement of genetic material from one organism into the genome of another species, is very common in microbes and is a major way that bacteria can acquire antibiotic resistance," said Claude dePamphilis, professor of biology at Penn State and senior author of the study. "We don't see many examples of horizontal gene transfer in complex organisms like plants, and when we do see it, the transferred genetic material isn't generally used. In this study, we present the most dramatic case known of functional horizontal gene transfer ever found in complex organisms."
Parasitic plants like dodder cannot live on their own by generating energy through photosynthesis. Instead, they use structures called haustoria to tap into a host plant's supply of water and nutrients. Dodder wraps itself around its host plant, growing into its vascular tissue, and often feeds on multiple plants at one time. It can parasitize many different species, wild plants as well as those of agricultural and horticultural importance.
"Parasitic plants live very intimately in connection with their host, extracting nutrients," said dePamphilis. "But they also get genetic material in the process, and sometimes they incorporate that material into their genome. Previous studies focused on single transferred genes. Here, we used genome-scale datasets about gene expression to determine whether the large amount of genetic material coming over through horizontal gene transfer is actually being used."
The research team identified 108 genes that have been added to dodder's genome by horizontal gene transfer and now seem to be functional in the parasite, contributing to haustoria structure, defense responses, and amino acid metabolism. One stolen gene even produces small segments of RNA known as micro RNAs that are sent back into the host plant, acting as weapons that may play a role in silencing host defense genes.
The team used rigorous criteria to determine whether the stolen genetic material was likely to be functional: The genes had to be full length, they had to contain all the necessary parts of a gene, they had to be transcribed into an RNA sequence that later builds proteins, and they had to be expressed in relevant structures. The team also explored the evolution of these transferred genes as additional support for functionality.
"We compare a gene's genetic sequence with closely related genes, and look for a special signature in how that sequence evolves to tell if it's likely to be functional," said dePamphilis. "Certain kinds of mutations in a gene do not affect the protein that the gene codes for and therefore do not impact the gene's function. When we see large amounts of these kinds of mutations, as opposed to mutations that might change or disrupt the gene's function, it is strong evidence that natural selection is acting to keep the proteins intact and useful."
Eighteen of the 108 genes appear in all dodder species, suggesting that these genes were originally stolen by the ancestral form of dodder and are maintained in modern species.
"This is the first time any study has seen evidence that horizontal gene transfers occurred early in the evolution of a parasitic group," said dePamphilis. "In this case, 18 of these genes were present in the common ancestor of all the living dodder species, which may have contributed to successful spread of these parasites."
The team also identified 42 regions in the dodder genome that appear to result from horizontal gene transfer, but do not have any functional genes.
"Because such a huge quantity of genetic material has come over through horizontal gene transfer, we suspect that the parasitic plants cannot filter what is coming in," said dePamphilis. "But natural selection is helping maintain the useful genes and filter out the less useful segments."
The researchers are currently investigating how exactly genetic material is being transferred from host to parasite. They would also like to explore whether this transfer is a one-way street, or if the host can obtain genetic material from its parasite.
"We'd love to know how extensive horizontal gene transfer really is," said dePamphilis. "We looked at just one of species of dodder, which is just one of over 4000 species of parasitic plants. Does horizontal gene transfer of functional genes happen to the same extent in other species? Is it possible in non-parasitic plants? In other complex organisms? This may be the tip of the iceberg."
In addition to dePamphilis the research team includes first author Zhenzhen Yang, a graduate student in the Plant Biology Graduate Program at Penn State at the time of the research, as well as Penn State researchers Eric Wafula, Saima Shahid, Paula Ralph, Prakash Timilsina, Wen-bin Yu, Elizabeth Kelley, Huiting Zhang, Thomas Nate Person, Naomi Altman, and Michal Axtell; Joel McNeal at Kennesaw State University; and Virginia Tech researchers Gunjune Kim and co-corresponding author James Westwood. This work was funded in part by the National Science Foundation and the United States and Department of Agriculture. Additional support was provided by the National Institute of Food and Agriculture, the Penn State Department of Biology, and the Penn State Huck Institutes of the Life Sciences.
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Materials provided by Penn State. Note: Content may be edited for style and length.
Journal Reference:
- Zhenzhen Yang, Eric K. Wafula, Gunjune Kim, Saima Shahid, Joel R. McNeal, Paula E. Ralph, Prakash R. Timilsena, Wen-bin Yu, Elizabeth A. Kelly, Huiting Zhang, Thomas Nate Person, Naomi S. Altman, Michael J. Axtell, James H. Westwood, Claude W. dePamphilis. Convergent horizontal gene transfer and cross-talk of mobile nucleic acids in parasitic plants. Nature Plants, 2019; DOI: 10.1038/s41477-019-0458-0
GENETIC AWARENESS IN ADAPTATION
Phylosymbiosis is a host-microbiome association in which the evolutionary tree of the host parallels the ecological changes in their microbial communities.
Credit: Bordenstein Laboratory, Vanderbilt University
Each animal species hosts its own, unique community of microbes that can significantly improve its health and fitness.
That is the implication of a laboratory study that investigated four different animal groups and their associated microbiota. The research found that each species within the group has a distinctive microbial community.
Additional experiments with two of the groups -- one mammal and one insect -- demonstrated that individuals possessing their natural microbiota digested food more efficiently and had greater survival than those that were implanted with the microbial communities of closely related species.
"Previous research has tended to concentrate on the negative effects of microbes. In this case we are showing that whole communities of microbes have positive effects as well," said Vanderbilt graduate student Andrew Brooks, co-first author of the study.
The paper describing the study's results is titled "Phylosymbiosis: Relationships and Functional Effects of Microbial Communities across Host Evolutionary History" and it was published Nov. 18 in the journal PLOS Biology.
"We coined the term phylosymbiosis a couple of years ago to denote the fact that evolution can act on host species and change their microbial communities," said Seth Bordenstein, associate professor of biological sciences and pathology, microbiology, and immunology at Vanderbilt University, who directed the study. Postdoctoral researcher Kevin Kohl and Robert Brucker at Harvard University were other co-first authors, and another participant, Edward Van Opstal, is a graduate student at Vanderbilt.
All animals teem with thousands of different species of microbes collectively called the microbiome. Biologists are actively investigating the extent to which these invisible communities play a significant role in the host animal's life and evolution. Answering this question is complicated by a number of factors including environment, diet, age, sex, host genetics and the wide variety of behaviors of the microbial species involved.
In the attempt to unravel the evolutionary relationship between hosts and their microbiomes, the Vanderbilt biologists investigated four groups of animals: deer mice, fruit flies, mosquitoes and jewel wasps.
First, the researchers characterized the microbiota of 24 closely related species in the four groups. Then they used statistical analyses to determine that the microbial communities form a "tree of life" that parallels that of their hosts. They also applied the same analysis to existing data on the microbiomes of great apes and found a similar pattern.
"The evidence indicates that the relationship between hosts and microbiomes is not always random but can be shaped by host evolution," said Bordenstein.
Next the biologists raised colonies of deer mice and jewel wasps in the laboratory under highly controlled conditions. In each group, they transplanted the microbiomes from closely related species into some of the individuals and then compared how rapidly they grew and how long they lived compared to those who had their microbiota removed and those that retained their natural set of microbes.
In this fashion, they discovered that when the microbial communities from house mice and different deer mice species were transplanted into one species of deer mouse, its ability to digest food was significantly reduced. As a result, they had to eat more mouse chow to get the energy they required.
Similarly, when jewel wasps received transplants of microbial communities from related wasp species, they had lower survival rates than those that had their natural microbiota.
"Plants and animals evolved in a planet dominated by microbial life," said Bordenstein. "So they had no choice but to tolerate microbes and, as we are now discovering, they also evolved the capacity to 'garden' them in order to enhance their health and fitness."
Story Source:
Materials provided by Vanderbilt University. Original written by David Salisbury. Note: Content may be edited for style and length.
Journal Reference:
Andrew W. Brooks, Kevin D. Kohl, Robert M. Brucker, Edward J. van Opstal, Seth R. Bordenstein. Phylosymbiosis: Relationships and Functional Effects of Microbial Communities across Host Evolutionary History. PLOS Biology, 2016; 14 (11): e2000225 DOI: 10.1371/journal.pbio.2000225
GENOMIC PLASTICITY AT THE BEGINNING OF MULTI-CELLULAR LIFE
One of the most exciting discoveries in genome research was that the last common ancestor of all multicellular animals -- which lived about 600 million years ago -- already possessed an extremely complex genome. Many of the ancestral genes can still be found in modern day species (e.g., human). However, it has long been unclear whether the arrangement of these genes in the genome also had a certain function. In a recent study in Nature Ecology and Evolution, the biologists led by Oleg Simakov and Ulrich Technau show that not only individual genes but also these gene arrangements in the genome have played a key role in the course of animal evolution.
Genomes store the instructions for how to build an organism. Often only individual genes are associated with certain functions. However, the genome not only defines single genes but also tells us about their arrangement on the DNA. Remarkably, many of these arrangements have been preserved from the genome of the common ancestor of sponges and humans, over 600 million years ago. Despite this, their potential function has long eluded scientists.
What gene arrangements reveal
In their current study, the team from the Department of Molecular Evolution and Development at the University of Vienna has now uncovered the first insights into this question. Using comparative genomic analyses, the researchers reconstructed evolutionarily conserved gene arrangements in animals and investigated their activity in different cell types. They could show that genes that are always present together in the genome in several species, also tend to be active in the same cells. For example, three genes that have been adjacent in several species (e.g., in sponges or cnidarians) for 600 million years are primarily active in a digestive cell type. "Cell types in animals can thus be characterized not only by individual genes but also by specific gene arrangements, and different cell types are also capable of accessing different regions in the genome," explains Oleg Simakov, evolutionary biologist at the University of Vienna. In addition, the team noted that certain cell types seem to utilize such conserved regions more than others, and thus may represent very ancestral functions.
The results show that not only gene loss or the emergence of new genes have played an important role in evolution, but also the changes in the arrangement of genes in the genome have made a significant contribution. "The study thus opens up a far-reaching perspective on investigating the functions of these regions in the respective cell types," concludes Simakov.
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Materials provided by University of Vienna. Note: Content may be edited for style and length.
Journal Reference:
- Bob Zimmermann, Nicolas S. M. Robert, Ulrich Technau, Oleg Simakov. Ancient animal genome architecture reflects cell type identities. Nature Ecology & Evolution, 2019; DOI: 10.1038/s41559-019-0946-7
NASH EQUILIBRIUM WINNING GROUPS FROM LOSING INDIVIDUALS
Inspired by the flashing Brownian ratchet, Parrondo's paradox is a counter-intuitive phenomenon in which two losing games, when played in a specific order, can surprisingly end up winning. For example, slot machines are designed to ensure that players lose in the long run. "What the paradox says is that there might be slot machines which are subtly linked in such a way that playing either slot machine independently will lead to financial disaster, but switching in between them will eventually leave the player richer than before," said senior author, Assistant Professor Kang Hao Cheong of the Singapore University of Technology and Design (SUTD).
To explore the plethora of exciting applications in biology, researchers from SUTD have examined a large range of recent developments of Parrondo's paradox in biology, across ecology and evolution, genetics, social and behavioral systems, cellular processes, and disease.
Their study, appearing in a recent issue of BioEssays, has identified key connections between numerous seemingly disjointed works, culminating in an emergent pattern of nested recurrent mechanics that appear to span the entire biological gamut, from the smallest of spatial and temporal scales to the largest. The authors explained that the pivotal role the paradox plays in the shaping of living systems has become increasingly apparent, which points strongly towards its potential identity as a universal principle underlying biological diversity and persistence.
"Developments in Parrondo's paradox to date have revealed a potential unifying fundamental characteristic of life itself, more valuable to our understanding of nature than its individual components," said co-author Jin Ming Koh.
The picture that the authors paint of biological reality is a striking one. Their work suggests that the biosphere might be supported by countless layers of Parrondo?paradoxical effects, each ingesting inevitably losing strategies and producing enhanced outcomes at a slightly larger temporal or spatial scale for the layer above, in what may be visualized as a fractal?like recurrent pattern. Such an imagery offers a fresh perspective on our view of nature and of ourselves.
The trio is now attempting to analyze the detailed structure of these mechanisms, which might span from hugely macroscopic spatial scales of entire ecosystems to the molecular inner workings of cells, and from the million?year timescales of evolution to sub-microsecond genetic and molecular processes. "Every cell, organism and species, and species assemblage and ecosystem, is necessarily mortal, yet the biosphere persists," said Assistant Professor Cheong.
Story Source:
Materials provided by Singapore University of Technology and Design. Note: Content may be edited for style and length.
Journal Reference:
Inspired by the flashing Brownian ratchet, Parrondo's paradox is a counter-intuitive phenomenon in which two losing games, when played in a specific order, can surprisingly end up winning. For example, slot machines are designed to ensure that players lose in the long run. "What the paradox says is that there might be slot machines which are subtly linked in such a way that playing either slot machine independently will lead to financial disaster, but switching in between them will eventually leave the player richer than before," said senior author, Assistant Professor Kang Hao Cheong of the Singapore University of Technology and Design (SUTD).
To explore the plethora of exciting applications in biology, researchers from SUTD have examined a large range of recent developments of Parrondo's paradox in biology, across ecology and evolution, genetics, social and behavioral systems, cellular processes, and disease.
Their study, appearing in a recent issue of BioEssays, has identified key connections between numerous seemingly disjointed works, culminating in an emergent pattern of nested recurrent mechanics that appear to span the entire biological gamut, from the smallest of spatial and temporal scales to the largest. The authors explained that the pivotal role the paradox plays in the shaping of living systems has become increasingly apparent, which points strongly towards its potential identity as a universal principle underlying biological diversity and persistence.
"Developments in Parrondo's paradox to date have revealed a potential unifying fundamental characteristic of life itself, more valuable to our understanding of nature than its individual components," said co-author Jin Ming Koh.
The picture that the authors paint of biological reality is a striking one. Their work suggests that the biosphere might be supported by countless layers of Parrondo?paradoxical effects, each ingesting inevitably losing strategies and producing enhanced outcomes at a slightly larger temporal or spatial scale for the layer above, in what may be visualized as a fractal?like recurrent pattern. Such an imagery offers a fresh perspective on our view of nature and of ourselves.
The trio is now attempting to analyze the detailed structure of these mechanisms, which might span from hugely macroscopic spatial scales of entire ecosystems to the molecular inner workings of cells, and from the million?year timescales of evolution to sub-microsecond genetic and molecular processes. "Every cell, organism and species, and species assemblage and ecosystem, is necessarily mortal, yet the biosphere persists," said Assistant Professor Cheong.
Story Source:
Materials provided by Singapore University of Technology and Design. Note: Content may be edited for style and length.
Journal Reference:
- Kang Hao Cheong, Jin Ming Koh, Michael C. Jones. Paradoxical Survival: Examining the Parrondo Effect across Biology. BioEssays, 2019; 41 (6): 1900027 DOI: 10.1002/bies.201900027
GENOMIC PLASTICITY AND THE NASH EQUILIBRIUM
Rapid evolution of other species happens all around us all the time -- and many of the most extreme examples are associated with human influences.
In a theme issue of the scientific journal Philosophical Transactions of the Royal Society B, researchers from McGill University have helped pull together the latest research on this phenomenon. The theme issue shows how humans affect the evolution of other species, and how those evolutionary changes can influence human societies. In many cases, these effects play out over only a few years to decades -- more quickly than biologists traditionally thought possible.
"Evolution is occurring all around us all the time, and it is influencing our environment, our health, and our overall well-being" says Andrew Hendry, professor in the Redpath Museum and Department of Biology at McGill University, and one of the editors of the theme issue.
When humans are involved, selection pressures on a species often become very strong, leading to fast evolution.
Consider three examples:
Commercial fishing. When fishing pressure is high, the fish evolve to reproduce when they are younger and smaller, and thus tend to have fewer, smaller offspring. This evolutionary change can, in turn, reduce fisheries yields and the sustainability.
Invasive species. The movement of species to new places in the world instigates evolution in those invasive species, which increases their rate of spread and impact on native species. Those native species can then sometimes evolve in response, potentially arresting the invader's spread and mitigating its impact.
Urbanization. The development of cities dramatically changes many aspects of the environment and, hence, can instigate evolution in a variety of species. As examples, plants evolve decreased seed dispersal to compensate for the expansion of uninhabitable pavement, animals evolve resistance to industrial and residential chemicals, and bacteria evolve resistance to antibiotics.
The collection of studies in the theme issue provides a rallying point for broader discussions of how human influences shape evolution and how that evolution, in turn, influences species traits, biodiversity, and "ecosystem services" -- the benefits that nature provides to humans, such as food, water and clean air.
"Evolution will fundamentally alter how species and ecosystems respond to environmental change," Hendry says. "Evolution therefore needs to be an integral part of our assessments of biodiversity and ecosystem services."
Story Source:
Materials provided by McGill University. Note: Content may be edited for style and length.
Journal Reference:
Kiyoko M. Gotanda, Andrew P. Hendry, and Erik Svensson. Human influences on evolution, and the ecological and societal consequences. Philosophical Transactions of the Royal Society B, December 2016 DOI: 10.17863/CAM.6418
SOMATIC MUTATION AND GENOMIC PLASTICITY
The towering, hundred-year-old Sitka spruce trees growing in the heart of Vancouver Island's Carmanah Valley appear placid and unchanging.
In reality, each one is packed to the rafters with evolutionary potential.
UBC researchers scraped bark and collected needles from 20 of these trees last summer, sending the samples to a lab for DNA sequencing. Results, published recently in Evolution Letters, showed that a single old-growth tree could have up to 100,000 genetic differences in DNA sequence between the base of the tree, where the bark was collected, and the tip of the crown.
Each difference represents a somatic mutation, or a mutation that occurs during the natural course of growth rather than during reproduction.
"This is the first evidence of the tremendous genetic variation that can accumulate in some of our tallest trees. Scientists have known for decades about somatic mutations, but very little about how frequently they occur and whether they contribute significantly to genetic variation," said Sally Aitken, the study's lead researcher and a professor of forestry at UBC. "Now, thanks to advances in genomic sequencing, we know some of the answers."
The researchers chose the Sitka spruce because it's among the tallest trees growing in the Pacific Northwest, and sampled the exceptional trees in Carmanah Walbran Provincial Park.
"Because these trees live so long and grow so tall, they're capable of accumulating tremendous genetic variation over time," explained Vincent Hanlon, who did the research as part of his master of science in the faculty of forestry at UBC.
"On average, the trees we sampled for the study were 220 to 500 years old and 76 metres tall. There's a redwood tree in California that's 116 metres tall, but these Sitka spruce were pretty big."
The researchers say more time and further studies will be needed to understand exactly how the different somatic mutations will affect the evolution of the tree as a species.
"Most of the mutations are probably harmless, and some will likely be bad," explained Aitken. "But other mutations may result in genetic diversity and if they're passed onto offspring they'll contribute to evolution and adaptation over time."
Studying somatic mutation rates in various tree species can shed light on how trees, which can't evolve as rapidly as other organisms like animals due to their long lifespans, nonetheless survive and thrive, Aitken said.
"We often see tree populations that adapt well to local climates and develop effective responses to changing stresses such as pests and bugs," she added. "Our study provides insights on one genetic mechanism that might help make this possible."
Story Source:
Materials provided by University of British Columbia. Note: Content may be edited for style and length.
Journal Reference:
- Vincent C. T. Hanlon, Sarah P. Otto, Sally N. Aitken. Somatic mutations substantially increase the per-generation mutation rate in the conifer Picea sitchensis. Evolution Letters, 2019; DOI: 10.1002/evl3.121
RAPID EVOLUTION OF NEW SPECIES
Biologists have discovered that the evolution of a new species can occur rapidly enough for them to observe the process in a simple laboratory flask.
In a month-long experiment using a virus harmless to humans, biologists working at the University of California San Diego and at Michigan State University documented the evolution of a virus into two incipient species -- a process known as speciation that Charles Darwin proposed to explain the branching in the tree of life, where one species splits into two distinct species during evolution.
"Many theories have been proposed to explain speciation, and they have been tested through analyzing the characteristics of fossils, genomes, and natural populations of plants and animals," said Justin Meyer, an assistant professor of biology at UC San Diego and the first author of a study that will be published in the December 9 issue of Science. "However, speciation has been notoriously difficult to thoroughly investigate because it happens too slowly to directly observe. Without direct evidence for speciation, some people have doubted the importance of evolution and Darwin's theory of natural selection."
Meyer's study, which also appeared last week in an early online edition of Science, began while he was a doctoral student at Michigan State University, working in the laboratory of Richard Lenski, a professor of microbial ecology there who pioneered the use of microorganisms to study the dynamics of long-term evolution.
"Even though we set out to study speciation in the lab, I was surprised it happened so fast," said Lenski, a co-author of the study. "Yet the deeper Justin dug into things -- from how the viruses infected different hosts to their DNA sequences -- the stronger the evidence became that we really were seeing the early stages of speciation."
"With these experiments, no one can doubt whether speciation occurs," Meyer added. "More importantly, we now have an experimental system to test many previously untestable ideas about the process."
To conduct their experiment, Meyer, Lenski and their colleagues cultured a virus -- known as "bacteriophage lambda" -- capable of infecting E. coli bacteria using two receptors, molecules on the outside of the cell wall that viruses use to attach themselves and then infect cells.
When the biologists supplied the virus with two types of cells that varied in their receptors, the virus evolved into two new species, one specialized on each receptor type.
"The virus we started the experiment with, the one with the nondiscriminatory appetite, went extinct. During the process of speciation, it was replaced by its more evolved descendants with a more refined palette," explained Meyer.
Why did the new viruses take over?
"The answer is as simple as the old expression, 'a jack of all trades is a master of none'," explained Meyer. "The specialized viruses were much better at infecting through their preferred receptor and blocked their 'jack of all trades' ancestor from infecting cells and reproducing. The survival of the fittest led to the emergence of two new specialized viruses."
Meyers's study was conducted over six years in two separate labs. The first experiments were performed at Michigan State, supported in part by BEACON, the National Science Foundation's Center for the Study of Evolution in Action, and the analyses were completed at UC San Diego.
Story Source:
Materials provided by University of California - San Diego. Original written by Kim McDonald. Note: Content may be edited for style and length.
Journal Reference:
J. R. Meyer, D. T. Dobias, S. J. Medina, L. Servilio, A. Gupta, R. E. Lenski. Ecological speciation of bacteriophage lambda in allopatry and sympatry. Science, 2016; DOI: 10.1126/science.aai8446
HORIZONTAL GENETIC TRANSFER WITH GENOMIC PLASTICITY AND AWARENESS
Many of an organism's traits are influenced by cues from the organism's environment. These features are known as phenotypically plastic traits and are important in allowing an organism to cope with unpredictable environments.
But what are the genetic mechanisms underlying these traits?
Jennifer Brisson, an associate professor of biology at the University of Rochester, and her former postdoctoral student Benjamin Parker, now an assistant professor of microbiology at the University of Tennessee, studied phenotypically plastic traits in pea aphids and uncovered, for the first time, genes that influence whether aphids produce wingless or winged offspring in response to their environment. In a new paper in the journal Current Biology, the researchers shed light on how phenotypically plastic traits evolve and address critical questions about the evolution of environmentally sensitive traits.
Pea aphids are insects that reproduce rapidly and typically give birth to offspring that do not have wings. As many gardeners know, aphids can quickly overwhelm and kill the host plants on which they live and feed. When an environment becomes too crowded with other aphids, the females begin producing offspring that have wings, rather than the typical wingless offspring. The winged offspring can then fly to and colonize new, less crowded plants.
"Aphids have been doing this trick for millions of years," Brisson says. "But some aphids are more sensitive to crowding than others. Figuring out why is key to understanding how this textbook example of phenotypic plasticity works."
The researchers used techniques from evolutionary genetics and molecular biology to identify genes that determine the degree to which aphids respond to crowding. Surprisingly, the genes they uncovered are from a virus that then became incorporated into the aphid genome. The virus, which is from a group of insect viruses called densoviruses, causes its host to produce offspring with wings. Researchers believe the virus does this in order to facilitate its own dispersal. As Brisson and Parker found, the gene from the virus retained the same function of producing winged offspring even after it was transferred and incorporated into the aphid genome.
"This is a novel role for viral genes that are co-opted by the genome for other purposes, like modulating plastic phenotypes," Parker says. "Microbial genes can become incorporated into animal genomes, and this process is important to evolution."
Most laterally transferred DNA -- DNA that is inherited from other organisms, like viruses -- is not expressed by its hosts because it is quickly inactivated or eliminated. However, there are examples in most organisms -- even humans -- where genomes co-opt genes laterally; in humans, for instance, the gene that creates a membrane between the placenta and the fetus was co-opted from a retrovirus.
Brisson and Parker found a clear case in which genes from outside an organism were co-opted by the organism's genome to modify the strength of a plastic response to environmental cues. Microbial genes like those from viruses can, therefore, play an important role in insect and animal evolution, Brisson says. "Even in ancient traits like the one studied here, new genes can start to play a role in shaping plastic traits and can help organisms cope with an unpredictable world."
Story Source:
Materials provided by University of Rochester. Original written by Lindsey Valich. Note: Content may be edited for style and length.
Journal Reference:
Many of an organism's traits are influenced by cues from the organism's environment. These features are known as phenotypically plastic traits and are important in allowing an organism to cope with unpredictable environments.
But what are the genetic mechanisms underlying these traits?
Jennifer Brisson, an associate professor of biology at the University of Rochester, and her former postdoctoral student Benjamin Parker, now an assistant professor of microbiology at the University of Tennessee, studied phenotypically plastic traits in pea aphids and uncovered, for the first time, genes that influence whether aphids produce wingless or winged offspring in response to their environment. In a new paper in the journal Current Biology, the researchers shed light on how phenotypically plastic traits evolve and address critical questions about the evolution of environmentally sensitive traits.
Pea aphids are insects that reproduce rapidly and typically give birth to offspring that do not have wings. As many gardeners know, aphids can quickly overwhelm and kill the host plants on which they live and feed. When an environment becomes too crowded with other aphids, the females begin producing offspring that have wings, rather than the typical wingless offspring. The winged offspring can then fly to and colonize new, less crowded plants.
"Aphids have been doing this trick for millions of years," Brisson says. "But some aphids are more sensitive to crowding than others. Figuring out why is key to understanding how this textbook example of phenotypic plasticity works."
The researchers used techniques from evolutionary genetics and molecular biology to identify genes that determine the degree to which aphids respond to crowding. Surprisingly, the genes they uncovered are from a virus that then became incorporated into the aphid genome. The virus, which is from a group of insect viruses called densoviruses, causes its host to produce offspring with wings. Researchers believe the virus does this in order to facilitate its own dispersal. As Brisson and Parker found, the gene from the virus retained the same function of producing winged offspring even after it was transferred and incorporated into the aphid genome.
"This is a novel role for viral genes that are co-opted by the genome for other purposes, like modulating plastic phenotypes," Parker says. "Microbial genes can become incorporated into animal genomes, and this process is important to evolution."
Most laterally transferred DNA -- DNA that is inherited from other organisms, like viruses -- is not expressed by its hosts because it is quickly inactivated or eliminated. However, there are examples in most organisms -- even humans -- where genomes co-opt genes laterally; in humans, for instance, the gene that creates a membrane between the placenta and the fetus was co-opted from a retrovirus.
Brisson and Parker found a clear case in which genes from outside an organism were co-opted by the organism's genome to modify the strength of a plastic response to environmental cues. Microbial genes like those from viruses can, therefore, play an important role in insect and animal evolution, Brisson says. "Even in ancient traits like the one studied here, new genes can start to play a role in shaping plastic traits and can help organisms cope with an unpredictable world."
Story Source:
Materials provided by University of Rochester. Original written by Lindsey Valich. Note: Content may be edited for style and length.
Journal Reference:
- Benjamin J. Parker, Jennifer A. Brisson. A Laterally Transferred Viral Gene Modifies Aphid Wing Plasticity. Current Biology, 2019; DOI: 10.1016/j.cub.2019.05.041
HORIZONTAL GENETIC TRANSFER SHAPING EVOLUTION
When viruses infect us, they can embed small chunks of their genetic material in our DNA. Although infrequent, the incorporation of this material into the human genome has been occurring for millions of years. As a result of this ongoing process, viral genetic material comprises nearly 10 percent of the modern human genome. Over time, the vast majority of viral invaders populating our genome have mutated to the point that they no longer lead to active infections. But, as scientists funded by the National Institutes of Health have demonstrated, they are not entirely dormant.
Sometimes, these stowaway sequences of viral genes, called "endogenous retroviruses" (ERVs), can contribute to the onset of diseases such as cancer. They can also make their hosts susceptible to infections from other viruses. However, scientists have identified numerous cases of viral hitchhikers bestowing crucial benefits to their human hosts -- from protection against disease to shaping important aspects of human evolution, such as the ability to digest starch.
Protecting Against Disease
Geneticists Cedric Feschotte, Edward Chuong and Nels Elde at the University of Utah have discovered that ERVs lodged in the human genome can jump start the immune system.
For a virus to successfully make copies of itself inside a host cell, it needs molecular tools similar to the ones its host normally uses to translate genes into proteins. As a result, viruses have tools meticulously shaped by evolution to commandeer the protein-producing machinery of human cells.
Feschotte and his team recognized that because viruses tend to attack the immune system, they may be particularly adept at manipulating immune system genes. Ancient human genomes may have evolved in response. Feschotte believes it is possible that the genomes of humans (or our ancient ancestors) repurposed viral DNA for their own defense, using it to spur the immune system into action against viruses and other foreign invaders.
"We hypothesized that these ERVs were likely to be primary players in regulating immune activity because viruses themselves evolved to hijack the machinery to control immune cells," says Feschotte.
To investigate their hypothesis, Feschotte and his team used a gene-editing technique called CRISPR to systematically eliminate individual ERV sequences in human cells. After removing one of the sequences, the researchers observed a notable weakening of immune function when the cells were challenged by viral infection. The removal of three other ERV sequences also compromised the immune response.
These findings suggest that each of these ERV elements can activate different gene components of the immune system. The team believes there are thousands more ERV sequences with similar regulatory activities, and it hopes to explore them systematically in future studies.
"We think we've only scratched the surface here on the regulatory potential of ERVs," says Feschotte.
Underscoring the complicated relationship humans have with viruses, strong evidence also exists that in some cases ERVs cause cancer but in other cases they protect against cancer. For example, an ERV called ERV9 can detect cancer-related damage in the DNA of cells in the testis. ERV9 then prompts a neighboring gene to induce the damaged cells to commit suicide. This protective mechanism ensures that the cancer cells will not spread.
Shaping Human Evolution
Scientists have also discovered that viral intruders have driven the evolution of human physiological functions ranging from early development to digestion.
Nearly 20 years ago, scientists identified an ERV-derived gene called syncytin that appears to play a key role in the development of the human placenta. Syncytin originated from a retroviral gene encoding a protein that is embedded in the outer surface of a virus. This protein mediates the fusion of the virions with the host cell membrane, thereby facilitating viral infection. In a remarkable turn of events, the human body has repurposed the viral protein's cell-fusing activities to promote the formation of the layer of cells that merge the placenta and the uterus.
Scientists have also found that viral invaders are critical to humans' ability to digest starch. The insertion of an ERV near the human pancreatic gene for making amylase -- a protein that helps humans digest carbohydrates -- led to the expression of amylase in saliva. The consequent ability to digest starch in the mouth has had profound effects on the human diet, notably a shift toward eating foods like rice and wheat. By helping to kick start digestion in the mouth, amylase relieves some of the burden of breaking down food faced by the small intestine. If this critical enzyme were not excreted in saliva, the small intestine would have more difficulty metabolizing sugars and starches.
More recently, in 2016, a team of U.S. and Israeli researchers reported that a common strategy that host organisms use for nullifying viruses -- bombarding them with mutations -- has helped shape human evolution.
The researchers, led by computational biologist Alon Keinan of Cornell University, in collaboration with Erez Levanon from Bar-Ilan University, study a virus-fighting family of human enzymes called APOBECs. During periods when DNA unzips into two single strands -- when it has been damaged, is in the process of being copied, or is being transcribed into RNA -- the APOBEC enzymes seek out bits of viral DNA. They then systematically strafe the viral DNA -- typically swapping many instances of one DNA base for another -- in order to neutralize pathogens lurking within the host genome.
It's likely that this APOBEC mechanism has also mutated non-viral portions of the human genome. Keinan says the majority of these genetic changes would have done enough damage to cause disease. For the most part, such mutations have been weeded out of the population because they were harmful to survival and reproduction. However, researchers have increasingly linked APOBECs to various cancers.
Keinan's team has shown that these mutations are also occurring in cells that develop into sperm and eggs and so they are inherited by future generations. And not all of the mutations have been detrimental. The genetic changes that survived through evolutionary time -- the ones that did not lead to disease -- are more likely to be beneficial. This insight suggests that the APOBEC anti-viral mechanism has helped shape primate evolution through a variety of yet-to-be-identified beneficial mutations. Keinan's team has reported tens of thousands of such mutations in hominid genomes and is now searching for specific examples that led to changes in function that have contributed to human evolution.
While the search for additional examples of beneficial ERVs and antiviral mechanisms continues, scientists are learning more about viral trespassers with the help of large databases of genomic information from numerous species. They're trying to figure out how viral DNA integrates into host genomes, how ERVs can jump from one host species to another and how to protect people in the case of these rare, but occasionally deadly, events.
Story Source:
Materials provided by NIH, National Institute of General Medical Sciences (NIGMS). Note: Content may be edited for style and length.
When viruses infect us, they can embed small chunks of their genetic material in our DNA. Although infrequent, the incorporation of this material into the human genome has been occurring for millions of years. As a result of this ongoing process, viral genetic material comprises nearly 10 percent of the modern human genome. Over time, the vast majority of viral invaders populating our genome have mutated to the point that they no longer lead to active infections. But, as scientists funded by the National Institutes of Health have demonstrated, they are not entirely dormant.
Sometimes, these stowaway sequences of viral genes, called "endogenous retroviruses" (ERVs), can contribute to the onset of diseases such as cancer. They can also make their hosts susceptible to infections from other viruses. However, scientists have identified numerous cases of viral hitchhikers bestowing crucial benefits to their human hosts -- from protection against disease to shaping important aspects of human evolution, such as the ability to digest starch.
Protecting Against Disease
Geneticists Cedric Feschotte, Edward Chuong and Nels Elde at the University of Utah have discovered that ERVs lodged in the human genome can jump start the immune system.
For a virus to successfully make copies of itself inside a host cell, it needs molecular tools similar to the ones its host normally uses to translate genes into proteins. As a result, viruses have tools meticulously shaped by evolution to commandeer the protein-producing machinery of human cells.
Feschotte and his team recognized that because viruses tend to attack the immune system, they may be particularly adept at manipulating immune system genes. Ancient human genomes may have evolved in response. Feschotte believes it is possible that the genomes of humans (or our ancient ancestors) repurposed viral DNA for their own defense, using it to spur the immune system into action against viruses and other foreign invaders.
"We hypothesized that these ERVs were likely to be primary players in regulating immune activity because viruses themselves evolved to hijack the machinery to control immune cells," says Feschotte.
To investigate their hypothesis, Feschotte and his team used a gene-editing technique called CRISPR to systematically eliminate individual ERV sequences in human cells. After removing one of the sequences, the researchers observed a notable weakening of immune function when the cells were challenged by viral infection. The removal of three other ERV sequences also compromised the immune response.
These findings suggest that each of these ERV elements can activate different gene components of the immune system. The team believes there are thousands more ERV sequences with similar regulatory activities, and it hopes to explore them systematically in future studies.
"We think we've only scratched the surface here on the regulatory potential of ERVs," says Feschotte.
Underscoring the complicated relationship humans have with viruses, strong evidence also exists that in some cases ERVs cause cancer but in other cases they protect against cancer. For example, an ERV called ERV9 can detect cancer-related damage in the DNA of cells in the testis. ERV9 then prompts a neighboring gene to induce the damaged cells to commit suicide. This protective mechanism ensures that the cancer cells will not spread.
Shaping Human Evolution
Scientists have also discovered that viral intruders have driven the evolution of human physiological functions ranging from early development to digestion.
Nearly 20 years ago, scientists identified an ERV-derived gene called syncytin that appears to play a key role in the development of the human placenta. Syncytin originated from a retroviral gene encoding a protein that is embedded in the outer surface of a virus. This protein mediates the fusion of the virions with the host cell membrane, thereby facilitating viral infection. In a remarkable turn of events, the human body has repurposed the viral protein's cell-fusing activities to promote the formation of the layer of cells that merge the placenta and the uterus.
Scientists have also found that viral invaders are critical to humans' ability to digest starch. The insertion of an ERV near the human pancreatic gene for making amylase -- a protein that helps humans digest carbohydrates -- led to the expression of amylase in saliva. The consequent ability to digest starch in the mouth has had profound effects on the human diet, notably a shift toward eating foods like rice and wheat. By helping to kick start digestion in the mouth, amylase relieves some of the burden of breaking down food faced by the small intestine. If this critical enzyme were not excreted in saliva, the small intestine would have more difficulty metabolizing sugars and starches.
More recently, in 2016, a team of U.S. and Israeli researchers reported that a common strategy that host organisms use for nullifying viruses -- bombarding them with mutations -- has helped shape human evolution.
The researchers, led by computational biologist Alon Keinan of Cornell University, in collaboration with Erez Levanon from Bar-Ilan University, study a virus-fighting family of human enzymes called APOBECs. During periods when DNA unzips into two single strands -- when it has been damaged, is in the process of being copied, or is being transcribed into RNA -- the APOBEC enzymes seek out bits of viral DNA. They then systematically strafe the viral DNA -- typically swapping many instances of one DNA base for another -- in order to neutralize pathogens lurking within the host genome.
It's likely that this APOBEC mechanism has also mutated non-viral portions of the human genome. Keinan says the majority of these genetic changes would have done enough damage to cause disease. For the most part, such mutations have been weeded out of the population because they were harmful to survival and reproduction. However, researchers have increasingly linked APOBECs to various cancers.
Keinan's team has shown that these mutations are also occurring in cells that develop into sperm and eggs and so they are inherited by future generations. And not all of the mutations have been detrimental. The genetic changes that survived through evolutionary time -- the ones that did not lead to disease -- are more likely to be beneficial. This insight suggests that the APOBEC anti-viral mechanism has helped shape primate evolution through a variety of yet-to-be-identified beneficial mutations. Keinan's team has reported tens of thousands of such mutations in hominid genomes and is now searching for specific examples that led to changes in function that have contributed to human evolution.
While the search for additional examples of beneficial ERVs and antiviral mechanisms continues, scientists are learning more about viral trespassers with the help of large databases of genomic information from numerous species. They're trying to figure out how viral DNA integrates into host genomes, how ERVs can jump from one host species to another and how to protect people in the case of these rare, but occasionally deadly, events.
Story Source:
Materials provided by NIH, National Institute of General Medical Sciences (NIGMS). Note: Content may be edited for style and length.
GENOMIC AWARENESS AND PLASTICITY IN THE NASH EQUILIBRIUM
, the best defense against hostile invaders is a good, long nap. Or at least, that strategy seems to work for bacteria.
In a new study, described in Nature, Rockefeller scientists showed that microbes under viral attack turn their defenses not only on their enemies, but also on themselves. This drastic measure, the researchers found, doesn't kill the bacteria, but rather sends them into a dormant state that prevents the infection from spreading.
Vicious viruses
Among bacteria, viruses called bacteriophages are public enemy number one.
These pathogens propagate by injecting their genome into unsuspecting microbes, eventually causing their host cell to rupture, at which point progeny phage is released to infect other members of a bacterial colony.
To mitigate these attacks, bacteria have evolved immune mechanisms known as CRISPRs, or clustered regularly interspaced short palindromic repeats, which, with the help of associated Cas enzymes, detect and destroy foreign genetic material.
Microbes have at their disposal many different CRISPR systems, one of which caught the attention of Luciano Marraffini due to its unique strategy for fending off intruders. Whereas most Cas enzymes destroy viral DNA, this particular enzyme, Cas13, works by cleaving RNA.
"Since Cas13 targets RNA, it was initially thought to have evolved to impede phages with RNA genomes. The problem is, RNA phages exceedingly rare," he says. "So we wanted to see whether it might have evolved to serve a different function."
Working with Helen Hay Whitney postdoctoral associate Alexander Meeske, Marraffini showed that activation of Cas13 actually protects bacteria from phages with DNA genomes, which are far more common. But how, they wondered, could an RNA-cutting enzyme actually defend microbes from this kind of virus?
Through a series of experiments, the researchers found that Cas13 helps bacteria, ironically, by hindering them. That is, the enzyme cuts up bits of host RNA, sending the bacteria into a dormant state -- a kind resting phase in which the microbes remain alive but don't grow. This strategy works, says Meeske, because viruses need host RNA to replicate.
"Phages are parasites: They don't have all the elements needed for their propagation, so they rely on the host," he explains. "And if the host cell isn't making those elements, the phage cannot propagate."
No escape
The researchers also found that Cas13 kills viruses more thoroughly than other Cas enzymes. Standard CRISPR-Cas systems are highly specific, cutting up bits of DNA that match a precise genetic sequence. And while this specificity can be an asset, it also comes with a big drawback: If a virus mutates, CRISPR cannot recognize the invader, and the phage escapes scot-free.
"If a phage has a single point mutation in its target sequence, then usually the virus is invisible to Cas and the infection will succeed," says Marraffini. "But with Cas13 we didn't see any escaper mutants."
The researchers attribute this superb virus-fighting power to the fact that cell dormancy does not target one particular virus, but rather makes it impossible for any phage -- including mutants -- to propagate. And while an indefinite nap may not seem like much of a life for a microbe, Meeske notes that the real benefit of Cas13 lies not at the level of the individual, but of the bacterial community as a whole.
"The phage has one shot to deliver its genetic payload and replicate," he says. "So if they inject their genome into a host that turns out to be inhospitable, the infection stops there. The phage loses, and the bacterial colony wins."
Story Source:
Materials provided by Rockefeller University. Note: Content may be edited for style and length.
Journal Reference:
- Alexander J. Meeske, Sandra Nakandakari-Higa, Luciano A. Marraffini. Cas13-induced cellular dormancy prevents the rise of CRISPR-resistant bacteriophage. Nature, 2019; DOI: 10.1038/s41586-019-1257-5
GENOMIC AWARENESS AND THE NASH EQUILIBRIUM
Bacteria can boost their own immune systems by "talking" to each other, surprising new research from New Zealand's University of Otago shows.
The findings by a team led by Associate Professor Peter Fineran of the Department of Microbiology and Immunology appear in the international journal Molecular Cell.
Associate Professor Fineran says that in the same way that humans are susceptible to viruses like influenza and measles, bacteria also need to defend themselves against viruses.
"As humans, we have evolved sophisticated immune systems that enable our bodies to fight the viral infections that render us ill. Amazingly, bacteria -- although single celled organisms -- often possess similar adaptive immunity called CRISPR-Cas systems. But the way that these CRISPR-Cas systems function is very much different to our own immune systems," he says.
His team's research provides new insight into how groups of bacteria collectively defend against viral threats.
"People have long understood the advantages of living in communities and bacteria are no different, often residing in close quarters to share resources. However, there are also potential drawbacks to community life as high-density bacterial populations are more vulnerable to the spread of viruses -- just like people in a crowded bus or a daycare centre," he says.
The breakthrough came when the researchers discovered that the ability of bacteria to gauge the number of cells in their communities enabled the bacteria to boost the power of their CRISPR-Cas immune systems to prevent viral outbreaks.
Associate Professor Fineran says the bacteria sense the population density by "talking" to each other using a form of chemical communication known as quorum sensing.
"The higher the population density, the stronger the communication between cells becomes, which results in greater coordination of immune defenses," he says.
Adrian Patterson, a PhD student and first author on the paper, says the study shows that bacterial cells preemptively elevate their immunity when they are most at risk of a virus spreading through the population.
"They both increase their ability to generate new immune memories and strengthen existing immunity by up to 500-fold," Mr Patterson says.
The role of CRISPR-Cas in providing bacteria with viral immunity was only discovered in the past decade.
The systems create genetic memories of specific past viral infections by taking little snippets of the viruses' DNA and storing them in memory banks to aid in recognising and destroying future infections.
One of the least understood aspects of the CRISPR-Cas field is how bacteria control the activity of these systems. Too much activity can result in an autoimmune-like disease, killing the host cell, but too little activity might allow viruses to wipe out entire bacterial communities. The team's research shows that by openly communicating with each other, bacteria strike the right balance between these two outcomes.
Dr Simon Jackson, second author of the study, says bacterial immune systems are fascinating to study.
"Lately we have made significant advances in understanding how they function. The really exciting part of our most recent discovery is that we predict the communication-based coordination of CRISPR-Cas immunity to be widespread throughout bacterial species."
Story Source:
Materials provided by University of Otago. Note: Content may be edited for style and length.
Journal Reference:
Adrian G. Patterson, Simon A. Jackson, Corinda Taylor, Gary B. Evans, George P.C. Salmond, Rita Przybilski, Raymond H.J. Staals, Peter C. Fineran. Quorum Sensing Controls Adaptive Immunity through the Regulation of Multiple CRISPR-Cas Systems. Molecular Cell, 2016; DOI: 10.1016/j.molcel.2016.11.012
GENOMIC PLASTICITY PROOF IN NASH EQUILIBRIUM
A biologist at Worcester Polytechnic Institute (WPI) has shown that a key biological component in a worm's communication system can be repurposed to take on a different job, a critical finding about the workings of evolution that could one day affect research into drug interactions, agricultural bio-engineering, and a better understanding of genetic inheritance through multiple generations.
Jagan Srinivasan, associate professor of biology and biotechnology at WPI, and his research team published their findings in Nature Communications, a peer-reviewed scientific journal. The paper, "Co-option of neurotransmitter signaling for inter-organismal communication in C. elegans," focuses on the evolution of the chemical communication components involved in inter-organismal signaling, which is essential for animals to navigate and survive in their natural environment.
"Evolution is intelligent, complicated, and opportunistic," said Srinivasan. "This was an old protein that the worm used for one thing and then, when a new need arose, used it for a novel function. It's more energy efficient to take something it already has and use it for a new function instead of creating something wholly new. Scientists had hypothesized about this kind of biological repurposing, but no one had shown it. We believe we are the first to show this repurposed receptor in the signaling system."
Neurotransmitters and neuroreceptors play a central role in biology, enabling cell-to-cell and animal-to-animal communication. For instance, in C. elegans, which are transparent nematodes widely used in biological and biomedical research, a neurotransmitter-sensing receptor, called TYRA-2, is needed for the worm's avoidance response to osas#9, a specific pheromone created during times of starvation. If a worm is starving, it will secrete osas#9, signaling to other worms to avoid the area because there's no food. Osas#9 and TYRA-2 work together for this avoidance response.
Funded in part by a $1.6 million National Institutes of Health grant received in 2017, Srinivasan's team has discovered that the nematodes repurpose the TYRA-2 receptor to bring about an aversive response, not between cells but among worms. This represents an inter-organismal communication pathway that evolved from inter-cellular neurotransmitter signaling via co-option of a neurotransmitter and its cognate receptor.
Other scientists had previously discovered that amino acid receptors can be re-purposed but Srinivasan's team is the first to show the repurposing of a neurotransmitter receptor. He will be studying whether other types of receptors can be repurposed, as well.
"This is not the end of the story. This is the tip of the iceberg," said Srinivasan. "This repurposing tells you how neurotransmitter signaling can evolve and how it affects the organism, whether it be humans, worms, or flies."
Over the course of more than four years of research that culminated in this Nature Communications paper, Srinivasan worked with Christopher Chute '18, PhD in Biology and Biotechnology; Douglas Reilly, PhD candidate in Biology and Biotechnology; and Veronica Coyle '16, undergraduate Biology and Biotechnology major; and with Elizabeth DiLoreto, research associate in his lab.
His team's discovery is now leading Srinivasan and his research lab to focus on three different, but related, areas that could be greatly affected by his re-purposing discovery.
The team is investigate how their finding about re-purposing could affect our understanding of drug interactions. A medication, for example, might have been created to target a specific disorder, like diabetes but by better understanding how someone's body might utilize the same neuroreceptor to use that same medication for a different function, scientists may better be able to determine the potential utility of off-target effects in the treatment of infectious diseases.
The WPI researchers also will study parasitic nematodes that attack plants, causing disease and crop and financial loss in the agricultural industry. For example, a report in Western Farm Press, a news site that focuses on agricultural production in California and Arizona, noted that soybean cyst nematodes are considered to be the most serious pathogenic threat to soybeans, and are estimated to reduce returns to U.S. soybean producers by close to $1 billion annually. Srinivasan is researching whether plants can be engineered to produce osas#9 as an adversive agent, sending out avoidance signals to cause nematodes to leave the plants alone, so farmers wouldn't need to use pesticide.
Srinivasan also is applying his findings to epigenetic research, the fairly new and quickly growing field of studying studying intergenerational (heritable) effects. Srinivasan, who has been working on research around how gene changes caused by environment and life changes are passed down through generations, now is studying how many generations of nematodes are affected by these changes.
"It looks like this receptor could cause epigenetic inheritance when you expose the mother to osas#9. Six generations of kids are sensitized to that," said Srinivasan. "Why does that happen? This data on repurposing is a big piece of that puzzle. We're putting pieces of the puzzle together."
Srinivasan worked with Frank Schroeder, professor of chemistry and chemical biology at Cornell University, to discover the osas#9 neurotransmitter in 2013.
Caenorhabditis elegans (C. elegans), which are used in Srinivasan's research, are transparent nematode worms that have a short lifespan, enabling scientists to conduct numerous observations and experiments in a relatively short period of time. Because the biological structures and processes being studied are common in all animals, work with C. elegans has implications for human health, aging and neurodegeneration.
Story Source:
Materials provided by Worcester Polytechnic Institute. Note: Content may be edited for style and length.
Journal Reference:
- Christopher D. Chute, Elizabeth M. DiLoreto, Ying K. Zhang, Douglas K. Reilly, Diego Rayes, Veronica L. Coyle, Hee June Choi, Mark J. Alkema, Frank C. Schroeder, Jagan Srinivasan. Co-option of neurotransmitter signaling for inter-organismal communication in C. elegans. Nature Communications, 2019; 10 (1) DOI: 10.1038/s41467-019-11240-7