The intellectual vacuity of New Scientist’s evolution issue: 3. The supposed importance of epigenetics in evolution

I’ll continue on with New Scientist‘s 13-section claim that the modern theory of evolution needs a reboot (see previous posts here and here), though I don’t know how much longer I can stand their uninformed palaver written by incurious journalists. Today we’l take up section 4: “There is more to inheritance than just genes”, which emphasizes the importance of epigenetic changes in evolution. The article appeared in this special issue of the rag magazine:

As I’ve written many times before, epigenetic changes are not good candidates for an inherited basis for evolutionary change, mainly because the vast majority of epigenetic modifications of DNA—usually via methylating DNA bases—disappear within one generation, as the DNA effaces the epigenetic markers during sexual reproduction. A few epigenetically produced traits can persist for a few generations, but that’s not a good basis for permanent evolutionary change, and certainly not a general explanation of adaptation. In fact, we know the genetic basis of adaptation in many cases, and it’s nearly 100% due to changes in the DNA sequence, not to epigenetic modification of the DNA sequence. (Lactose tolerance in pastoral human populations is one example.)

To support the claim that epigenetics is important in evolution, author Carrie Arnold mentions the shopworn example of pregnant Dutch women, deprived of food by the Nazis, giving birth to children who became unhealthy adults, with high levels of obesity, diabetes, and so on. Besides this not being an example of adaptive evolutionary change, it’s still not certain that the changes in the kids were produced by epigenetic modification of the DNA. The pregnant mothers were the ones who passed on the traits, and the fetuses could have been affected by the mother’s physiology, not by changes in her DNA. (It’s telling that the children of undernourished fathers alone didn’t show the changes.) There may have been some epigenetic changes, or maternal effects, in that the grandchildren seem to be affected too, but that’s where the train of changes comes to a stop.

Then Arnold mentions an experiment with which I wasn’t familiar, but supposedly demonstrated epigenetic changes that persisted for many generation—25, to be precise:

Subsequent studies in plants and animals suggest that epigenetic inheritance is more common than anyone had expected. What’s more, compared with genetic inheritance, it has some big advantages. Environments can change rapidly and dramatically, but genetic mutations are random, so often require generations to take hold. Epigenetic marks, by contrast, are created in minutes or hours. And because they result from environmental change, they are often adaptive, boosting the survival of subsequent generations.

Take the pea aphid. It is capable of both sexual and asexual reproduction, and comes in two varieties: winged and wingless. When scientists exposed a group of genetically identical pea aphids to ladybirds, the proportion of winged aphids increased from a quarter to a half. This adaptation, which helped them escape the predatory ladybirds, persisted for 25 generations. The aphid DNA didn’t mutate, the only change was epigenetic.

So I “took” the pea aphid, reading the paper that supposedly showed persistent epigenetic variation over 25 generations. Click on the screenshot below to get the paper (from the journal Heredity):

It’s a long and somewhat tedious read, but there are two points to make.

1.) The plastic response to the predator—growing wings (an adaptation that’s genetically encoded)—did not persist for 25 generations on its own. In fact, if you remove the predator, the stimulus for growing wings, the population becomes wingless again within a single generation. So we do not have a case of epigenetic markers persisting on their own for many generations, much less two generations.

2.) There is no evidence that the production of winged forms is caused by epigenetic modification of the DNA, and the authors admit this.

In other words, everything that Arnold says or implies about this experiment is misguided.

The experiment was started with a single clonal population of aphids, that is, parthenogenetically produced individuals from a single female. The population thus lacked genetic variation except for new mutations that could have occurred after the experiment started. One part of the population was the experimental section, exposed to predatory ladybirds. That one produced winged individuals immediately at a proportion of about 50% of the population. This proportion remained stable for 27 generations. Producing wings in the presence of predators is adaptive, of course, as you can flee them, and not producing wings when the predator is absent is also presumably adaptive, as there’s a metabolic and reproductive cost of producing wings you don’t use. Thus the switching between wings and winglessness is an adaptive plasticity, and is presumably coded (not epigenetically!) in the aphids’ DNA.

The control line, lacking ladybirds, stayed at about 25% winged individuals for 25 generations.

At three intervals, the authors took aphids from the experimental line and put them in an environment without predators. If the epigenetic markers persisted in the absence of the predator, and through meiosis, you’d expect these “reversion” lines to still show a higher frequency of winged individuals. They didn’t. They basically reverted to the control level of winglessness within a single generation, presumably because the switch for growing wings (ladybirds) wasn’t there.

So what we see is that to get the adaptive trait, wings, to persist, you need the stimulus to be there constantly. The presence of the predator somehow induces the aphids to grow wings, just as the presence of fish in a pond causes some rotifers to grow fish-repelling spines. And when you take the predator away, the aphids switch back to the wingless form. Here’s a plot showing the frequency of wings in the experimental population (red line), in the control predator-less population,  (black line) and the reverted population in which predators were removed (blue line):

Unlike the Dutch situation, or others that report persistence of environmentally induced changes for a few generations, in this case the induced change, the presence of wings, reverts to control levels within a generation. We do not see the kind of trait persistence here that epigenetics advocates tout as important in making the phenomenon important in evolution.

And indeed, we don’t even know if the switch from winglessness to wings is an epigenetic change, as opposed to some chemical change that occurs in the aphids when they sense the presence of predators that turns on “wing-making genes”. (That’s how it works in rotifers: when a fish eats a rotifer, it releases chemicals into the water that induce the other rotifers to produce spines. That’s not an epigenetic modification of the DNA.) If you think that any environmental change is “epigenetic”, then yes, this one could be, but that’s not the way the cool kids construe “epigenetic” these days. It’s taken to mean “alterations of the DNA structure”, which is what journalist Arnold means by mentioning “epigenetic marks [that] are created in minutes or hours.”

There’s one twist in the experiment as well: in the lines subject to predators, the plasticity of individuals became reduced; that is, they were less likely to respond to changes in predators with changes in wings. The paper’s authors impute this to epigenetics, but it could well be due to selection occurring on mutations that arose in the predator lines. That is, since predation was omnipresent, there was less selection pressure to maintain a “switching system,” and your plasticity could erode. To maintain a switch between wings and winglessness, the lineage has to experience periodic bouts of predation alternated with bouts of no predation. So the loss of plasticity itself also says nothing about whether epigenetic markers were accumulating in the DNA.

And, at the end, the paper’s authors admit that we don’t know whether this switch is due to epigenetic modification of the DNA, as the New Scientists reporter claims.  From the Heredity paper:

We can thus tentatively attribute the decline in plasticity observed in lines that were exposed to predators for many generations to the action of some non-genetically transmitted information (i.e. information not encoded in the DNA sequence). The hypothesis that observed phenotypic changes were caused by reversible epigenetic changes is thereby more likely but in order to be confirmed, this hypothesis would require to be backed up by molecular analyses.

I can find nothing in this paper that even suggests that epigenetic changes were happening to the aphids’ DNA, much less any kind of inherited changes that persist for more than one generation. This paper is certainly not an example of what New Scientist says it is.

This is the third buzzwordy phenomenon tendered by New Scientist as an exciting new finding that can modify the Modern Evolutionary Synthesis. And it’s the third one that is wrong. I am growing weary, and will see if I need to persist in debunking further claims in the article. Rest assured, though, that most of them are even weaker than the three I’ve discussed. But what does New Scientist care? They want clicks, not accuracy, and I fear that I’m wasting my time. I’d rather write about the new paper on consciousness in crows.

At least the New Scientist article admits that epigenetics is controversial:

The extent of epigenetic inheritance is contested. Some sceptics point out that, during mammalian reproduction, the creation of sperm and egg cells involves erasing epigenetic markers. Others argue that epigenetic transmission across generations is extremely widespread and useful. In plants, for example, it can account for differences in fruit size, flowering time and many other survival-boosting traits.

Yes, but it’s because the transmission across generations lasts about two or three generations at most that is why epigenetic modification by itself is not a good candidate for the “replicator” that produces adaptive evolution.

Lunchtime!