Many genes, but two major roads to adaptation

Cross-posted at Denim and Tweed.

In the course of adaptive evolution — evolutionary change via natural selection — gene variants that increase the odds of survival and reproduction become more common in a population as a whole. When we’re only talking about a single gene variant with a strong beneficial effect, that makes for a pretty simple picture: the beneficial variant becomes more and more common with each generation, until everyone in the population carries it, and it’s “fixed.” But when many genes are involved in adaptation, the picture isn’t so simple.

This is because the more genes there are contributing to a trait, the more the trait behaves like a quantitative, not a Mendelian, feature. That is, instead of being a simple question of whether or not an individual has the more useful variant, or allele, at a single gene — like a light switch turned on or off — it becomes possible to add up to the same trait value with different combinations of variants at completely different genes. As a result, advantageous alleles may never become completely fixed in the course of an adaptive evolutionary response to, say, changing environmental conditions.

That principle is uniquely well illustrated by a paper published in the most recent issue of Molecular Ecology, which pairs classic experimental evolution of the fruitfly Drosophila melanogaster with modern high-throughput sequencing to directly observe changes in gene variant frequencies during the course of adaptive evolution. It clearly demonstrates that when many genes contribute to adaptation, fixation is no longer inevitable, or even necessary.

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My gut microbiota made me do it!

Our bodies are teeming with bacteria: for every one human cell in your body, there are at least 10 microbial cells. That’s about 100,000,000,000,000 microbes – what are they all doing?

The communities of microorganisms that live on or in a particular host are called the microbiota, and are responsible for a lot of physiological and biochemical functions. It’s probably no surprise that the gut microbiota digest complex molecules we’ve eaten and they keep pathogens from colonizing our bodies (most of the time). They synthesize vitamins and amino acids that we can’t make ourselves. Recent studies have shown that variation in gut microbiota are associated with obesity, diabetes, normal brain development and insulin signaling (which has a downstream affects on body size and developmental rate). But there’s one effect that variation in microbiota can have on their host that is particularly fascinating to me: they can influence host mate choice.

In 1989, Diane Dodd reared fruit flies (Drosophila pseudoobscura) from a common stock on two different food sources: starch and maltose. She found that after multiple generations of isolation on their separate substrates, starch-flies preferred to mate with starch-flies and maltose-flies preferred to mate with maltose-flies. The result was robust and repeatable, but the reason why and its mechanism were unknown.

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