DNA methylation is the term for a modification to certain DNA bases that involves the addition of a methyl group. This slows down gene expression, which may or may not be advantageous in context – though if you remove it entirely in mice you kill them outright. To cut to the chase, in late August a paper – Divergent Whole-Genome Methylation Maps of Human and Chimpanzee Brains Reveal Epigenetic Basis of Human Regulatory Evolution (pdf, supplemental data) – came out comparing levels of methylation, concentrating on the brain, between humans and chimpanzees. They found differences, particularly in regions apparently associated with diseases that we suffer from more than chimps do. Here’s a figure stolen from their supplemental information:
“NS” stands for “not significant,” but the ones with stars are. Something to note with that graph is that there is a hidden 20% below the axis, so the differences are not quite as large as they would appear.
Brian Thomas’ article – and it is Brian, even though you might have expect Jeff Tomkins here – is called Stark Differences Between Human and Chimp Brains. His point basically boils down to the following claim:
If humans and chimps are close relatives, then they should have similar DNA methylation patterns in the areas of chromosomes that they have in common such as similar gene sequences. However, this team found major differences.
How does he know that? The abstract to the paper states:
To date, it remains largely unknown how patterns of DNA methylation differ between closely related species and whether such differences contribute to species-speciﬁc phenotypes.
Even in those species that even creationists like Brian have to admit are related we don’t actually know how similar their methylomes are. We also don’t know how easily it can change with evolution. With that in mind, we can’t say that “If humans and chimps are close relatives, then they should have similar DNA methylation patterns in the areas of chromosomes that they have in common such as similar gene sequences.”
Thomas does try to justify claiming that the differences are too large for what should be expected:
A second observation is that the very genes that were differently methylated “exhibit striking associations with several disorders, including neurological and psychological disorders and cancers.” These data show that methylation patterns in many cases can tolerate very little disruption, thus presenting another impossible hurdle for the evolutionary model to overcome.
No, that’s not a reasonable conclusion. For one, looking at the data for different samples in the paper there is a fair bit of variation even within humans:
(First three (“HS”) bars are human, other three (“Y”) are chimp. Note again the constricted y-axis scale. The X chromosome is circled as the only female sample (HS813) has significantly lower methylation than the others. I’m not sure exactly how the extra chimp chromosome is factored in here, I assume it’s just labelled by where the genes fit on the human chromosomes.)
Given these results it would be more reasonable to conclude that the increased gene expression we gain from less methylation simply comes at a cost, and not that the levels are entirely inflexible. Thomas’ conclusion is therefore entirely unjustified:
If humans evolved from chimpanzee-like creatures, then some unknown evolutionary process must have altered their methylomes. But since methylomes apparently cannot tolerate that much alteration, then the evolutionary story must be in error.
There is much that is not known about methylation, and epigenetics in general. But this fact also means that you can’t rule out a lot, either – certainly not evolution as a whole.