[Centraal] Evolutie in het nieuws

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Op dinsdag 1 september 2009 10:47 schreef Triggershot het volgende:
Racisten, eet je hart uit.
[..]

http://www.nu.nl/wetensch(...)0-jaar-geleden-.html

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Genes That Make Us Human

Finding genes that have evolved in humans among our genome's 3 billion bases is no easy feat. But now, a team has pinpointed three genes that arose from noncoding DNA and may help make our species unique.

Most genes have deep histories, with ancestors that reach down into the tree of life, sometimes all the way back to bacteria. The gradual increase from the few thousand genes in a bacterium to the tens of thousands of genes in a person came primarily through genome- and gene-duplication events, which created extra sets of genes free to evolve new sequences and new functions. Much of this duplication happened long before humans evolved, though some duplications occurred in the human lineage to create exclusively human twins of existing genes.

But in 2006, geneticists showed for the first time that they could identify truly novel genes. In fruit flies, they came across five young genes that were derived from "noncoding" DNA between existing genes and not from preexisting genes. As a result, other researchers started looking for novel genes in other species.

Meanwhile, while looking for gene duplications in humans, geneticists Aoife McLysaght and David Knowles of Trinity College Dublin kept coming across genes that seemed to have no counterparts in other primates, suggesting that new genes arose in us as well. To determine which of these genes with no counterparts were de novo genes, McLysaght and Knowles first used a computer to compare the human, chimp, and other genomes. They eliminated all but three of the 644 candidates because their sequence in the database was not complete--or they had equivalents in other species.

Next, they searched the chimp genome for signs of each gene's birth. "We strove hard to identify the noncoding DNA that gave rise to the gene," McLysaght says. Only by finding that DNA could they be sure that the gene wasn't already present in the chimp genome but was somehow unrecognizable to gene-finding programs. At three locations where the chimp and human genomes were almost identical, telltale mutations indicated that it was impossible to get a viable protein from the chimp DNA sequence. In contrast, the human version of each sequence had mutations that made it a working gene, the researchers report online tomorrow in Genome Research.

The researchers were able to verify that the genes worked by checking messenger RNA databases and protein surveys done by other scientists. They are now using antibodies to find out where in the cells these proteins are active and are trying to disable the genes in cells to tease out their functions.

The researchers analyzed only a subset of the human genome. Extrapolating to the full genome, they think humans have evolved at least 18 new genes. That's a small number compared to our total of 24,000 but nonetheless an important one. "The distinction between humans and other apes must lie somewhere in the small genetic differences between the species," says McLysaght.

Unlike duplicated genes, these are genes that "they really knew are human-specific," says Laurent Duret, a molecular evolutionary biologist at the University of Lyon in France. When he first heard about this project, he was skeptical, but not anymore. "It's the first convincing evidence of a real innovation in humans."

These three young genes join several hundred other uniquely human genomic features, including gene duplications, that provide tantalizing hints of what makes us human. But, says evolutionary biologist Gregory Wray of Duke University in Durham, North Carolina, researchers still have no clue what most of these genes do.

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Googling Food Webs: Can an Eigenvector Measure Species' Importance for Coextinctions?

A major challenge in ecology is forecasting the effects of species' extinctions, a pressing problem given current human impacts on the planet. Consequences of species losses such as secondary extinctions are difficult to forecast because species are not isolated, but interact instead in a complex network of ecological relationships. Because of their mutual dependence, the loss of a single species can cascade in multiple coextinctions. Here we show that an algorithm adapted from the one Google uses to rank web-pages can order species according to their importance for coextinctions, providing the sequence of losses that results in the fastest collapse of the network. Moreover, we use the algorithm to bridge the gap between qualitative (who eats whom) and quantitative (at what rate) descriptions of food webs. We show that our simple algorithm finds the best possible solution for the problem of assigning importance from the perspective of secondary extinctions in all analyzed networks. Our approach relies on network structure, but applies regardless of the specific dynamical model of species' interactions, because it identifies the subset of coextinctions common to all possible models, those that will happen with certainty given the complete loss of prey of a given predator. Results show that previous measures of importance based on the concept of “hubs” or number of connections, as well as centrality measures, do not identify the most effective extinction sequence. The proposed algorithm provides a basis for further developments in the analysis of extinction risk in ecosystems.

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Rapid Evolution of Functional Complexity in a Domain Family

Multicellular organisms rely on complex, fine-tuned protein networks to respond to environmental changes. We used in vitro evolution to explore the role of domain mutation and expansion in the evolution of network complexity. Using random mutagenesis to facilitate family expansion, we asked how versatile and robust the binding site must be to produce the rich functional diversity of the natural PDZ domain family. From a combinatorial protein library, we analyzed several hundred structured domain variants and found that one-quarter were functional for carboxyl-terminal ligand recognition and that our variant repertoire was as specific and diverse as the natural family. Our results show that ligand binding is hardwired in the PDZ fold and suggest that this flexibility may facilitate the rapid evolution of complex protein interaction networks.

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Time always marches forward — and so does evolution, according to a new study showing that protein changes that happened over the course of tens of millions of years can prevent molecular turnarounds and render evolution irreversible.

"This backwards pathway is not accessible to selection," says study author Joe Thornton, a molecular evolutionary biologist at the University of Oregon in Eugene. "It's very strongly supported evidence for the view that contingency plays a major role in evolution."

More than a century ago, the French–born Belgian palaeontologist Louis Dollo proposed that evolution cannot retrace its steps to restore a lost trait — an idea that has remained controversial. Dubbed Dollo's law, this proposition had a certain appeal to many evolutionary biologists. Whales and snakes never regained legs, for example; birds did not reacquire teeth. But more recently, studies have shown that silenced genes and dormant developmental programs can be reactivated, leading many researchers to believe that evolution can indeed double back on itself.

Evolution's arrow

Thornton and his colleagues decided to test Dollo's law at the molecular level. They focused on the glucocorticoid receptor (GR), a protein that binds the hormone cortisol to regulate the stress response and other functions in humans and other vertebrates. Thornton's team had previously showed that the first GR protein evolved more than 400 million years ago from an ancestral receptor that was activated by a trio of hormones: cortisol, aldosterone and deoxycorticosterone1. Over the course of 40 million years, the ancestral protein acquired 37 amino-acid alterations, cortisol binding to produce the 'modern' GR protein2.

The researchers reverse-engineered the protein to undo all seven mutations that affected cortisol binding, but the resulting receptor was non-functional and did not bind any hormone. To determine whether other mutations might be having an effect on receptor function, the team looked at the three-dimensional structure of the protein and pinpointed five additional mutations. These extra mutations did not affect the cortisol-binding specificity of the receptor but they did prevent it from doing its job properly. When the researchers reversed these mutations as well, the protein was transformed back into its ancestral functional state and could bind all three hormones.

Although it is technically possible for the molecular changes to backtrack, admits Thornton, such a shift couldn't be driven by natural selection. Undoing the five extra mutations in the absence of the other seven changes had negative or neutral consequences on protein function, and so would not be favoured by evolution, the researchers report in Nature3. "The chances of reversibility ever happening are vanishingly small," Thornton says. "It's virtually impossible."

Traces of time

The study reveals how interdependencies between amino acids can limit the scope of evolution, says Günter Wagner, an evolutionary developmental biologist at Yale University. "Because [the additional mutations] are only enabling but not themselves selective, they can mutate away, effectively burning the bridge you went over," he says.

Michael Rose, an evolutionary biologist at the University of California, Irvine, says that the experimental demonstration of irreversibility was "impressive" but not all that surprising. "That this phenomenon would apply on this timescale is what every evolutionary biologist would expect," he says. But in the short term, selection often goes back to its old ways. For example, earlier this year, Rose and his colleagues showed that fruit flies that had diverged over decades of selection in the lab returned to their ancestral state after just two years of reverse selection4. Thornton's study, by contrast, "is way, way macro in time frame," Rose says, adding, "It illustrates the importance of historicity in evolutionary biology."

But Fyodor Kondrashov, an evolutionary geneticist at the Centre for Genomic Regulation in Barcelona, Spain, disagrees. "There's absolutely nothing impossible about reversing everything that has happened," he says. Rather than focusing on the authors' "spin of reversibility", Kondrashov says, the paper highlights how the likelihood of particular evolutionary trajectories is contingent on a protein's genetics and structure. "We really need these kinds of examples", he adds.