The latest issue of Science contains two papers (references below) worth reading. Sadly, both are behind paywalls, but judicious inquiry might yield a pdf). One, a short perspective by Simon Fisher and Matt Ridley, emphasizes that a lot of genetic changes supposedly responsible for major features human evolution—like the highly-touted FOXP2 gene, whose evolution was supposedly the cause of human speech,since mutations in the gene degrade human speech and that gene evolved quickly on the hominin branch of the ape lineage—might have evolved quickly only after cultural innovations or changes in other genes allowed the supposedly “responsible” genes to evolve in concert with that other change.

An example of culture-driven genetic evolution is the rapid evolution of lactose tolerance genes in human populations, which I recount in WEIT. In the descendants of human “pastoral” populations (that is, those groups who kept sheep, goats, or cows for milk), we observed the rapid evolution of lactose tolerance within the last 10,000 years. Most humans are lactose tolerant as infants: we have to be, because we drink milk. But as infants age and get weaned, the genes allowing them to break down the lactose milk sugars got turned off, for milk-drinking wasn’t a feature of early human populations. As humans domesticated animals for milk, a cultural change, there arose powerful selection pressures to not turn off those genes so that we could derive continued nutrition from those milk sugars. (The selection pressure is estimated at an astounding 10%, meaning that those individuals who could digest milk left 10% more offspring than those whose tolerance genes remained turned off.) This cultural change of keeping milk animals, then, caused a rapid genetic evolution of permanent “on” genes in several populations. This is known as “gene-culture coevolution.”

Fisher and Ridley make the point that the rapid evolution of FOXP2 could mean not that evolution at that gene enabled humans to use language, but simply refined our abilities to use sophisticated vocal communication after it had already developed via earlier genetic and cultural evolution. Or, FOXP2 could have nothing to do with language at all, but simply reflect some other form of selection.

Their argument makes sense, and I like it because I also raised doubts about the FOXP2 story in WEIT. Geneticists and evolutionists are all too eager, when they find a gene that has evolved rapidly in the human lineage, to speculate that this is the gene responsible for some innovation “that makes us human.” Fisher and Ridley simply note that the rapid evolution could be a consequence rather than a cause of something that had already evolved—be it culturally or genetically.

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The second story is amazing, demonstrating the old evolutionary bromide in the title. When an animal becomes resistant to something that humans use to poison it, it usually evolves to detect that poison and avoid it, or become physiologically resistant to it (as bacteria become resistant to antibiotics or mosquitoes to DDT). But in the case of the German cockroach (Blattella germanica), it’s done something more clever: it’s somehow re-jiggered its taste system so that the attractant that humans used to draw the insect to poison bait—the sugar glucose—now tastes bitter to the roach, and they avoid it.

Before the mid-1980s, roach control experts would spray poisons on everything to control roaches. That didn’t go down very well with people, and so the companies switched to baits, which included not only a poison, but something to attract the roaches to the deadly baits: the sugars D-glucose and D-fructose, which roaches love. (Sucrose, our table sugar, is a dimeric molecule that links fructose to glucose.) But within a few years, cockroaches began appearing that avoided the baits, and did so not because they were averse to the poison, but because they were averse to the attractant, glucose. This new trait turned out to be heritable, that is, it had a genetic basis.

Ayako Wade-Katsumata and coauthors hypothesized that the aversion to glucose was a result of evolution in the way the taste buds and brain detected and perceived the sugar.

To figure this out, they wired up nerve cells (neurons) in the cockroaches’ taste receptors (“taste sensilli”), which reside in hairs around the mouth. The figure below, from the paper, shows those hairs and the kind of single hair whose nerve cells (those cells that detect and respond to stimulants) could be wired up to see if the nerve cells fire when exposed to different molecules. (It’s amazing what neurophysiologists can do these days). There are several types of taste receptors in the hairs, but the authors concentrated on two: those that, when they fire, send a signal to the sweet detector in the brain, and those cells whose firing sends signals to the bitter detector in the brain. In normal, unselected roaches, only the first cells fire when the beast tastes glucose, stimulating it to feed. When the bitter receptors cause the bitter neurons to fire, the roaches avoid what they’ve tasted.

(Caption from Fig. 1 of paper). Side view of the right paraglossa of a WT [“wild type”, i.e. not glucose-averse] male cockroach (left, maxillary and labial palps were removed), and a taste sensillum used in electrophysiological recordings (right).

What the authors found is that in cockroaches that had evolved to avoid baits, glucose stimulated the firing not only of glucose receptors, but also the bitter receptors. (The positive response of the sweet receptors to glucose was also lower in bait-averse cockroaches than in normal, wild-type cockroaches.) In other words, what once attracted the roaches to baits now repelled them.

The authors don’t yet know the genetic and neurological details of how this happened. As they note, it could be caused by structural changes in the “bitter’ receptor molecules so that they now detect glucose but send signals to the bitter neurons, causing aversion. Alternatively, there could have been mutations that put glucose-detectors on the bitter-tasting neurons, so that they’d fire in response to glucose, but send “ecch” signals to the brain.

The lesson from this, besides being the usual cautions that evolution is unpredictable, and that natural selection can often favor striking and unexpected responses, is that taste, like every other sense, reflects a combination of external stimuli and neuronal wiring that tells the brain how the brain interprets those stimuli. Something being “tasty” or “repugnant” is not an inherent quality of a food but of the combination of food and how it stimulates the taste receptors and brain. Receptors can evolve in a way that makes something that once tasted great now taste horrible, or vice versa. (That goes for odors, too.) I’ve always said that rotting meat probably tastes as good to a vulture as an ice-cream sundae does to us. (And if you don’t like ice-cream sundaes, you’re reading the wrong site!)

h/t: Linda Grilli

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References:

Wada-Katsumata, A., J. Silverman, and C. Schal. 2013. Changes in taste support the emergence of an adaptive behavior in cockroaches. Science 340:972-975.

Fisher, S. E and M. Ridley. 2013. Culture, genes, and the human revolution. Science 340:929-930.