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Evolution’s tricky shortcuts

Such incidents may have happened repeatedly during evolution, some researchers believe.

This exploitation of foreign genes for an organism’s own benefit also may exemplify a wider phenomenon on which scientists are beginning to shed light: evolution takes what seem to be ingenious “shortcuts” to advance itself faster.

When Charles Darwin first proposed the theory of evolution in 1859, he made it clear the process was slow and painful. According to the modern version of the theory, organisms occasionally pick up random mutations. The tiny fraction of mutations that are helpful, as opposed to harmful, help their bearers live longer and multiply more widely. This leads to the emergence of new species by gradual steps – one rare, tiny, risky mutation at a time.

The sheer difficulty of this process has helped fuel opposition to Darwin’s theory since its inception. “The difficulty of accumulating and fixing variations,” wrote a famous Darwin opponent, Samuel Wilberforce, is what in part precludes “any promise of a true transmutation of species.”

But if recent findings are correct, evolution may have learnt to skip a few steps. It seems to have ingeniously found back-alleys and shortcuts through the labyrinth of molecular machinery that makes evolution itself possible. Some examples follow:

Gene repeats

A puzzle that has intrigued biologists since Darwin’s time is why the fossil record shows new species seem to emerge suddenly and rapidly – in contrast to the gradual process that evolution is supposed to be. Researchers at University of Texas Southwestern Medical Center, Dallas, Texas, found an explanation in dog genes.

The explanation would be that many mutations occur in regions of the genes where a single, simple instruction is repeated many times. The mutations involve removing or adding one repeat. This differs substantially from what most scientists have traditionally considered the predominant mechanism of mutations, which alters only one “letter” of code changes at a time – a much smaller change.

The difference is somewhat like an instruction manual’s editor mistakenly changing the number of times an instruction is repeated, as opposed to changing one letter in the book. The former action is more likely to meaningfully alter the final result.

The chemical units that make up an organism’s DNA, or genetic code, are abbreviated with the letters A, C, T and G. Strings of these letters spell out the genetic instructions needed to carry out life’s functions. Many scientists believe evolution occurs through “single-point” mutations – a change from one letter to another among the billions of letters in the code.

The researchers found that bigger changes occur in genetic regions, called tandem repeat sequences, consisting of the same series of letters repeated many times over, for example, ACTACTACT. These mutations happen in these regions when such units – the ACT in the above example – are mistakenly added or subtracted as a group.

The researchers found that such changes help explain the length of dogs’ muzzles. The scientists combined genetic data from different dog breeds and data on the shapes of dog skulls, and found that that the length of a dog’s muzzle depends on the number of times specific tandem repeat units determining muzzle length are repeated.

Mutations in tandem repeat sequences occur up to 100,000 times more often than single point mutations, and are much more likely significantly change physical appearance, said John “Trey” Fondon, an evolutionary biologist and co-author of the study.

“I was struck by the prevalence of very highly mutable tandem repeats in the coding regions of genes responsible for development,” he said. “That’s when it occurred to me that this may be an important mechanism whereby our genomes are able to create lots of useful variations in genes that are important for our development, our shape and structure, and our overall appearance.

“Many of the shape difference that we see in evolution are not suddenly adding a wing or a leg. They are distortions, the stretching or squishing of a body part,” he added. Tandem repeat sequences are also found in genes regulating brain development, an area where humans have evolved rapidly, the researchers added. The findings are published in the advance online edition of the research journal Proceedings of the National Academy of Sciences the week of Dec. 13.

“Promiscuous” proteins

Evolution is a gamble: to stay a step ahead of a shifting environment, organisms must change or risk extinction. Yet the instrument of this change, mutation, carries a serious threat: mutations are hundreds of times more likely to be harmful to the organism than advantageous. In a paper published online Nov. 28 in the research journal Nature Genetics, scientists showed one way that evolving organisms may be hedging their bets: “promiscuous” proteins.

Proteins are a type of complex molecule that carries out most of the day-to-day work of keeping us alive. Our genes’ job is mainly to specify how each protein is built.

Some proteins do only one thing, such as spurring a chemical reaction needed to break down food. But researchers are increasingly finding many, even most, proteins have more than one job. For example, a protein called PON1 mainly works to help clear the body of substances called lactones. But it also has side jobs: it helps remove cholesterol that can clog the arteries, and breaks down some pesticides.

These so-called “promiscuous” proteins can serve as ready-made starting points for the evolution of new functions, according to the researchers, at the Weizmann Institute of Science, Rehovot, Israel. Proteins’ “promiscuity” allows them to mutate slightly in such a way that they can take on new tasks without jeopardizing their principal function, reducing the risks inherent in evolution.

The institute’s Dan Tawfik and colleagues simulated a speeded-up version of evolution in the lab. This involved, in part, introducing random mutations into genes coding for various proteins. 

The result: the proteins changed considerably in the way they handled their extra, “promiscuous” activities, but changed very little in the way they carried out their primary function.

The proteins are in a sense hedging their bets, Tawfik said. “Two contradictory things are necessary” for evolution, he explained. On the one hand, an organism must undergo “as little change as possible in its functioning in spite of mutations.” On the other, evolution “requires some mutations to induce new traits. It appears that the organism can have it both ways: the main function remains robust while the promiscuous functions are extremely responsive to mutation.”

The scientists believe that promiscuity may be an intermediate phase for some evolving proteins. In the face of evolutionary pressure, a single protein could evolve into two distinct ones, Tawfik asserted.

This multi-tasking may also partly explain another phenomenon that puzzles biologists: rapidly emerging drug and antibiotic resistance, and enzymes that have adapted to break down man-made chemicals that have only existed for 50 years. Natural evolution, according to standard theory, should take thousands and hundreds of thousands of years to work, the scientists said.

Taming alien genes

Perhaps the most striking example of evolutionary shortcuts is the way organisms seem to have tamed alien genes.

Many of our genes aren’t our own at all: they are “selfish” genes that have somehow infiltrated. These genes, which probably infected our ancestors by way of viruses or other mechanisms, do little but replicate themselves. They spread inside our DNA depositing scraps of unwanted genetic code amid the useful stuff. “Selfish” genes contain code for the production of enzymes – types of proteins – that help replicate the gene.

But many organisms have apparently turned the tables on these selfish genes, subjugating them and converting them to their own uses.

Researchers at the Medical University of Vienna, Austria, recently found that people and chickens both contain a peculiar version of a selfish gene called “P transposons,” known to afflict many simpler organisms including insects and zebrafish.

But whereas P transposons exist in many copies in each insect and zebrafish – attesting to the gene’s ability to self-replicate – the corresponding chicken and human version exist in only one copy, the researchers found. This and other evidence suggests the higher organisms found a way to tame the rogue gene, the researchers wrote, in a process some scientists call “molecular domestication.”

The researchers described their findings in the Dec. 22 advance online edition of the research journal Molecular Biology and Evolution. The human and chicken versions of the gene create a protein that’s abundant throughout much of the body, suggesting it has an important function in metabolism, the researchers wrote. But what this function is remains unknown, they added.

The findings provided new evidence to boost a theory that researchers had proposed several years ago – that “molecular domestication” is a key source of evolutionary innovation.

If an organism succeeds in domesticating errant proteins by “taming their ‘anarchistic behavior,’ such an event can be considered as an important evolutionary innovation for its own benefit,” wrote the university’s Wolfgang Miller and colleagues in a paper in the research journal Genetica in 1999.

In fact, it seems such domestication “took place repeatedly,” in evolution, they added, and may even have been especially important in the beginning of life, when it was necessary to quickly stitch together bits of DNA from different sources to create a functional organism. Molecular domestication, they wrote, “might be considered as a resumption of the same evolutionary process that drove the transition from ‘primitive genomes’ to ‘modern’ ones at the early dawn of life.”

—EJL

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