There’s a movement afoot by money-hungry but misguided scientists to claim that the Modern Synthesis (MS) of evolutionary biology is fatally flawed. (Many of these researchers are funded by the John Templeton Foundation, which recently handed out $11 million dollars for work on this fruitless endeavor.)
According to the critics, the areas that supposedly have inflicted mortal wounds on the MS are niche construction, evolutionary developmental biology (“evo devo”), developmental plasticity, and, above all, epigenetics—the idea that evolutionary adaptation can be fueled by changes in the genome produced not by mutation altering the sequence of basis in the DNA, but alterations in the genome induced by the environment itself, like changes in the histone scaffolding of DNA or methylation of the DNA bases.
I’ve discussed these so-called fatal flaws before (e.g., here) and find them grossly overblown. They either limn phenomena that already fit comfortably within the MS, or propose scenarios that, while logically plausible, are supported by almost no evidence.
One of the latter is epigenetics, about which I hear incessantly. Does the environment actually induce changes in DNA methylation that can be the basis of adaptive change? The evidence for that is virtually nonexistent, for those changes usually disappear after one or a few generations, and thus cannot be the permanent heritable variation required for long-term adaptation.
This issue was recently discussed at length in a new paper in the Proceedings of the Royal Society, “The sources of adaptive evolution” (reference below; download not free but some judicious inquiry might yield a pdf). The paper was written by my good friends Deborah Charlesworth, Nick Barton, and Brian Charlesworth (the Charlesworths were colleagues in Chicago until deciding to return to the UK). The paper, which considers the evidence for epigenetic bases of adaptation, is written very clearly, a refreshing change from the postmodernist babble I’ve been inflicting on you lately.
The paper’s verdict: there’s little evidence for environmentally induced DNA or histone alterations that can fuel adaptive evolution, and the MS remains on solid footing. A few words from their conclusions (I’ve omitted the references, and the bolded bit is my doing):
Genetic studies of adaptive phenotypes have yielded several further important conclusions. First, there are now many examples of phenotypic differences within and between species whose genetic control maps to a small region, but with multiple nucleotide differences within the region being causally involved. This supports Darwin’s and Fisher’s view that adaptive phenotypes are usually built up by a series of relatively small changes, which has been challenged by proponents of the EES.
Second, phenotypes that show plastic responses to environmental conditions also often show considerable genetic variation in these responses, and DNA sequence variants associated with these heritable differences have been identified, supporting the view that plasticity has evolved in a neo-Darwinian fashion. For example, vernalization responses in flowering plants involve a period of exposure to cold that is required for seed germination. (This was the basis for the notorious Lamarckian theories of T. D. Lysenko, which seriously damaged Soviet agriculture.) Vernalization is under the control of a complex epigenetic regulatory system, which is reset each generation. Natural vernalization response differences are controlled by DNA sequence variation in cis-acting regulatory sequences.
In contrast with the rigorous empirical evidence for the role of DNA sequence variants in adaptive evolution that we have outlined, there is currently little evidence for effects of epigenetic changes, although more data are required. Recent claims for such effects have been based on evidence that changes affecting the methylome are more numerous than some types of sequence variants in evolving lineages of Darwin’s finches and darter fish. Such comparisons, however, provide no evidence that the epigenetic variants in question had any role in phenotypic evolution.
The paper also considers the notion of “directed mutation” or “adaptive mutation”, a truly non-MS concept, but finds virtually no evidence for such nonrandom changes in DNA. Other topics discussed (and critiqued) are “evolvability” and non-genetic “adaptive plasticity” as a basis for evolution.
It’s a good paper, even if it does buttress the status quo!
h/t: Bruce
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Charlesworth, D., N. H. Barton, and B. Charlesworth. 2017. The sources of adaptive variation. Proceedings of the Royal Society B: Biological Sciences 284.DOI: 10.1098/rspb.2016.2864
Naturally the Templeton Foundation is interested in any flaw in our mainstream understanding of evolution.
Any adaptations due to the environment means their god can poke his fingers into the mechanism by changing that environment.
Also any genetic variation is obviously god playing his evolution piano.
As a counter attack has any body considered cloning Darwin, Huxley or Hooker?
I think they would better understand the antiquated way Templetons think of science than we do.
I find particularly annoying the use of “epigenetics” to mean basically nothing more than “gene regulation” or “differential gene expression” while acting like this is a hot new field of study. I spent my whole academic career, beginning in the mid-1960s, studying gene regulation, and explicitly in an evolutionary context (i.e., what is the role of regulatory change in evolution?) from about 1978.
Very good! (But what does “EES” stand for?) Maybe “epigenetic evolution scenario”? (Displaying my ignorance here.)
“Extended evolutionary synthesis”, I think.
Yes, you’re correct. Templeton funded biologists like D.S. Wilson declare the Modern Synthesis dead and buried; one might say “repealed and replaced” by the EES. With a straight face they declare this as established fact, to which all credible biologists assent; with the notable exceptions of some ideological holdouts such as Richard Dawkins and Jerry Coyne. It’s crazy.
I do not understand most of the “long words” here -I was only a lorry driver! – but as for “epigenetics — the idea that evolutionary adaptation can be fueled by changes in the genome produced not by mutation altering the sequence of basis in the DNA, but alterations in the genome induced by the environment itself”, it was often reported that in the UK, during the nineteenth century and the first half of the twentieth century the plumage of birds with normally light-coloured feathers living in smoke-laden industrial cities turned dark to match both the smoky atmosphere and the dark dirty places where they roosted.
Now, with cleaner atmospheres, the change may have been reversed.
I hadn’t heard about the birds but the famous Peppered moth showed the same transition from lighter color before the industrial revolution to a darker form and back again once the air became cleaner. But this is not an example of epigenetic change; it is, in fact, prima facie evidence for Darwin’s idea of Natural Selection. The darker colored moths were harder for predators to spot against tree trunks darkened by soot, so predation pressures on the them were less than for lighter ones.
You don’t say whether the birds grew darker plumage, or simply acquired darker plumage from the dirty environment. Consider, for example, the lungs of people in smoke-laden industrial cities, which on post-mortem investigation proved to be much darker than those of people with cleaner air. (Independently of this, the lungs of smokers were darker than those of non-smokers.)
It does not seem to me that darker plumage would benefit the birds in these areas, and it seems very unlikely that darker lungs would be selected for.
This is good. And we should be heartened to see articles that push back against the careerists. They have been making so much noise and getting so much attention that ironically at this point one could make a name for oneself by simply defending the olde MS.
Yes, this is helpful. Some of the graduate students and postdocs in my research group are quite interested in epigenetics as a phenomenon and as a possible basis for adaptive evolution. Most of that interest is misplaced but it is hard to argue against because early-career researchers want to catch the next wave and epigenetics is wavy. This paper suggests that students would be better off catching a different wave.
“alterations in the genome induced by the environment itself”
To be honest, I’ve never understood how epigenetics enthusiasts imagine this is supposed to work. The environment itself can’t reach in and alter the genome directly by psychokinesis or spooky action at a distance. Any changes must be mediated by cellular machinery that evolved for that purpose. So what am I missing? Where’s the beef?
You’re not missing anything. You are correct – the mechanisms involved in inducing, controlling, maintaining and expressing epigenetic changes are themselves subject to MS type evolution, undermining a principle concept in those who think epigenesis is somehow different to evolution as we understand it.
Furthermore, during gametogenesis (production of sperm or eggs) the DNA that is made during meiosis does not contain bases modified by methylation. The *sequence* of the DNA can be modified during meiosis- this is mutation, the building blocks of evolution- but the bases are not copied using modified nucleotides. The modifications come later. How then are somatic modifications (the epigenetic modifications that occur in cells other than gametes) become encoded in the gametes if they don’t start out with them?
A fertilised egg is not simply a genome. It is a functioning cell with cytoplasm belonging to the mother. The chemicals in that cell, enzymes, RNAs, whatever, determine what parts of the genome are expressed during the first few divisions.
I was not referring to a fertilized egg. The genome of an egg or sperm is not expressed (it is haploid) and when meiosis occurs, the resulting daughter eggs or sperm do not contain modified bases. Those bases get modified later.
I know that epigenetic changes occur in the developing embryo and this is where epigenetic modification are made by maternal (but obviously not paternal) epigenetic pressures. The data suggests that the same bases modified in the mother can be modified in the embryo. This is also (as above) a regulated biochemical process; how is that directed and controlled? All the known players in this biochemical pathways are themselves subject to the MS. There is no need to invoke something new and unexplained.
I don’t think we have a real disagreement, and I suspect that you know more about the subject than I do. As you say, the bases get modified later. I wanted to stress the continuity from mother to zygote: as you say, the same bases modified in the mother can be modified in the embryo.
The other co-author Nicholas Barton wrote (with Briggs, Eisen, Goldstein and Patel) a very good 800+ page textbook “Evolution” that came out in 2007. All three authors know what they are talking about.
It’s interesting to note that the most ardent fans of the EES seem to also be SJWs.