Evolution, parasites, selection pressures, PZ Myers, and tangential infertility issues

If the title of this blog post seems awfully miscellaneous to you, let that be a warning: The post will be likewise.

Recently, I have read a lot of books on evolution and biology that talk about the role of parasites (and bacteria and other agents of disease) in evolution, most importantly two books: Carl Zimmer’s Parasite Rex (an excellent book, read this!) and Matt Ridley’s The Red Queen (also a good book, although I found it less riveting than Zimmer’s). Both of these books present or allude to the idea that parasites and infection have been immensely powerful driving forces behind evolution. In fact, this is a leading explanation for why sex exists (to mix up lock-and-key molecules in our immune system and confuse the efforts of parasites to evolve counters to our immune defences).

Personally, I accept this intellectually but find it hard to really take to heart; growing up with Sir David Attenborough I tend to think of selection pressures as, say, cheetahs hunting down Thompson’s gazelles—very clear and obvious what the pressures and consequences are for each participant. When contemplating ungulate evolution, a cheetah or a wolf looks like a much greater pressure than a cestode or a tick.

And of course books that go into detail on parasites will emphasise those points—Carl Zimmer’s book is called Parasite Rex, for crying out loud; of course he’ll focus on that, and even if he’s completely correct and honest I may come away with a bias toward the things he talks about because, well, that’s what my recent reading has been all about. So is the pressure so vast, or is my perspective biased by my selection of literature?

Well, the other day, having attended a talk at UBC, I happened to be sitting next to PZ Myers at the pub. This seemed like a golden opportunity to ask this question of a biologist who has read or studied evolution an awful lot—a biologist, furthermore, who as far as I know does not have a horse in the parasite race. The answer was enlightening and interesting. PZ told me that when you look at the human genome you can estimate what genes have been subject to most natural selection. As I understand it, you basically measure ratios of synonymous to non-synonymous changes.

An aside, as I understand it (PZ did not go into this in depth, but I believe it is fairly simple; correct me if I am wrong!). Synonymous change is a mutation where even if the gene is translated to protein, there is no change in function, e.g. because the change is between two amino acids that do the very same thing. (A non-synonymous change is, obviously, one where there is a change in function if the gene is transcribed.) If a gene is constrained by natural selection, it will tend to keep its function, while a gene with no selection pressures acting on it is free to vary randomly and will pick up non-synomymous mutations. In fact, scientists use junk DNA—DNA that is never translated to proteins—as a sort of genetic clock: Because the DNA doesn’t do anything, it will drift over time, picking up M mutations every N years, so you can measure how long two lineages have been split by checking how far their junk DNA has diverged.

Back to what PZ said, then. He told me that when you look at the human genome, there are two areas where almost all the changes have happened over the past several million years: The immune system, and genes for sperm recognition (by which the ovum knows to admit sperm and reject foreign matter like bacteria and fungal spores). Every other change is, by comparison, rare and incidental. This means two things: First, the parasites are primary forces in providing selection pressure notion is confirmed. Second…sperm recognition; what’s that?

Sperm recognition is a feature I had never heard about, but an extremely important one (as shown by the huge selection pressures). Women, of course, have various problems, one being that their reproductive tract offers a helpful avenue for pathogens to enter their bodies. Because ova are limited in number, they need to be protected. Therefore, it is extremely important that when they fuse with anything, it is a genuine fertilisation. It would be extremely maladaptive if ova fused with every bacterium or fungal cell that made its way to the Fallopian tubes before the immune system could get to them. Therefore, ova are equipped with chemical receptors that recognise various molecules on the coatings of sperm cells and allow only cells with valid ‘key’ molecules inside.

This, PZ said as an aside, is one common cause of difficulty conceiving. There’s a fair amount of polymorphism in the population: Two men’s sperm cells don’t carry the exact same complement of molecular keys to engage the chemical locks on the ova; two women’s ova don’t have the exact same chemical locks. In some rare cases, two perfectly fertile inviduals of opposite sex may be unfortunate enough that this particular man’s sperm carry a set of keys, and the woman’s ova a set of locks, but none of the keys fit the locks—even though each of them may be perfectly able to have children with most people, they cannot have children together.

This is what I learned over a beer with PZ Myers. Incidentally, I gave him an official Pope card. I got it a long time ago from wildmage and I was sad to part with it, but who better to hold papacy?