The selfish epigene

This is another archival repost from the old blog, originally from july 2007.

I started writing this over a month ago, but may have got a little distracted. I’m not entirely sure what point it was supposed to be making anymore, but I do remember that, because it was supposed to be an introduction to a series on some topic or other, I couldn’t write anything else for the blog until I finished this one.

I’ve been reading Julian Huxley’s Soviet Genetics and World Science, about Michurinism/Lysenkoism, a pseudo-scientific alternative to genetics that was official Soviet doctrine in the 1940s. Lysenkoism denied Mendelian genetics and Darwinian natural selection, in favour of a version of Lamarckism – the 19th century hypotheses that evolution occurs by the inheritance of acquired characteristics. The standard simplified explanation of the difference is that in evolution by natural selection, variation in giraffe neck length is heritable, and the taller giraffes get more food, and are therefore more likely to survive long enough to pass on the relevant genes in exactly the same state that they received them. In Lamarckism, giraffes stretch their necks, reaching for vegetation, and the result of the stretching gets passed on to their offspring. Lamarck was justified in proposing this hypothesis: at the time, genes had not even been discovered, so nobody could know that they can’t be modified by stretching your neck; Darwin himself did not rule out inheritance of acquired characteristics as an evolutionary mechanism.

However, by the 1940s it had become clear that Mendelian inheritance and Darwinian natural selection were, in the most part, true. In 1944, DNA was shown to be the location of genes, and it had been known for decades that chromosomes were the “organs of heredity”, as Huxley puts it. We now know an awful lot more about genes and the organs of heredity, and while the old rules still stand, we’ve discovered a lot of very interesting new ones as well. My current favourite is epigenetics. There are several different definitions of “epigenetics” floating around, so I best define what I mean. Epigenetics is inheritance that does not take the form of nucleotide sequences in DNA. The mechanisms of epigenetic inheritance vary, and I intend to explain a few in future entries. For now, all we need to know is that at least one of these mechanisms appears, at first sight, to provide a medium for the inheritance of acquired characteristics.

My particular interest in epigenetics is mostly concerned with its implications for development (more on that in future posts), because most epigenetic inheritance occurs somatically (i.e. within a multicellular organism, rather than between generations). Over at Wikipedia, though, Nbeale has been arguing that epigenetic inheritance across multiple generations is a refutation of the “selfish gene” theory of evolution. One’s answer to that could merely be to point out that epigenetics does not negate the fact that most inheritance remains nucleotidal in its nature. But how does epigenetic inheritance fit with the existing ideas anyway?

The particular example of the inheritance of acquired characteristics cited by Nbeale is a study that found a correlation between mortality and paternal grandparent early life nutrition (there is no elegant way of concisely explaining the study – I spent five minutes trying!). Nbeale also claims that Robert Winston used this as an example of the failings of “neo-Darwinism” and Richard Dawkins’ selfish gene theory, though I haven’t been able to view the original source to verify this. At first sight you might think that the paternal grandparental nutrition effect is an example of the inheritance of acquired characteristics. It is almost certainly not, and can be explained within the current paradigm – even in selfish gene terms if you wish.

I must at this point give a brief explanation of one mechanism of transgenerational (or ‘germ-line’) epigenetic inheritance. Genes can be silenced by being tightly wrapped in proteins called histones, which get in the way of the machinery of gene expression, preventing it interacting with the gene. To determine which genes get silenced this way, chemical modifications are made to the DNA which act as signals, and these signals are copied when the DNA is copied, thus being propagated in daughter cells and future generations. One example of this in germ-line epigenetic inheritance may include imprinting (though I don’t know for sure whether this mechanism can be said to be responsible for all cases of imprinting). We inherit two copies of each gene — one from each parent — and with imprinted genes, one copy is switched off. Imprinting is very orderly: the same set of genes are imprinted in all individuals, and for each of these genes, the sex of the parent we inherit the activate and inactive forms from is the same for everybody. However, in terms of mechanism, we can think of the paternal grandparental nutrition effect as being a sort of “on-the-fly” version of imprinting.

Evolution by natural selection does not proceed in a teleological fashion with a specific goal in mind. Natural selection works with the variation it is given, and therefore comes up with sub-optimal botch jobs, like the back-to-front vertebrate retina. There is no reason to believe that some epigenetic mediated inheritance of acquired characteristics would behave any differently: it would, like natural selection, have to make do with the variation it has. It is therefore very suspicious that the paternal grandparental nutrition effect occurs repeatedly at such a statistically significant rate that can be picked up by a study that didn’t know it was looking for any such effect in the first place. If this is an acquired characteristic that is being inherited, how come it’s acquired so often?

The reason that it is acquired so often, is almost certainly that there is an innate predisposition to that characteristic arising and being passed on, and certain environments (malnutrition) encourage this. And at this point we can pick up the problem, and look at it from another angle. The paternal grandparental nutrition effect on mortality is the phenotype of a gene (or genes). It is traditional genetics with a twist, and a similar twist to one that Dawkins (remember, NBeale dragged his name in, not me) wrote about in The Extended Phenotype, where he pointed out that phenotypes may be distinct or even distant from an individual’s physical body — from beaver dams to parasitic takeover of host behaviour. There are many different ways we can classify phenotypes, and lots of varied layers between gene and phenotype. It’s not always easy to recognise what’s what, or what influenced what, and a physiologist’s “cause” may be a molecular biologist’s “effect”. The phenotype may be a behavioural trait, the intermediate a neurotransmitter, encoded by a distinctly average gene. In our case, the phenotype is seen in grandchildren, and, off the top of my head, a mere two hypothetical intermediates are all it takes to link phenotype to hypothetical gene. The first is chemical modification of the DNA, thus altering its interaction with histones. The second is the enzyme that does the DNA modification. There is no reason to suspect the enzyme is anything other than average, and like all others, it is the product of a gene activated by a particular set of environmental circumstances — in this case, malnutrition. The evolutionary biologist’s cause and effect are epigentics and mortality, while the geneticist’s cause and effect are gene and enzyme. Sadly, I think that having slightly different perspectives on a subject may be the cause of the most vociferous and pointless arguments.

The details of this case may not be exactly as described above, but the important thing is, there is no reason to suspect that the paternal grandparental effect fundamentally contradicts the modern synthesis, or the selfish gene theory. As long as the gene(s) “for” this effect are average genes, they are subject to natural selection, and whatever your opinion of the selfish gene view of evolution, it is not epigenetics that is going to overthrow it. Now then, to the real substance of epigenetics…

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