relative selective pressure on human and chimp genomes

Pharyngula has a great post up about a study [PLoS] on selective forces on genes we share with chimpanzees, examining whether selection was favoring divergence between the two species at those genes. Turns out, the heaviest divergent selection was on genes for cancer supression and sperm production. The surprise is that there was little divergent selection on genes that are expressed in the brain.

[Note Added: you can read my full post after the fold, but really I just repeat PZ, so you should read him]


Here is PZ's lucid explanation of the technique:

One parameter that can be assayed is the frequency of synonymous changes in the DNA: these are changes in the nucleotide sequence that produce synonyms in the triplet code, and therefore cause no changes at all in the protein sequence. These changes represent a kind of steady background noise, the rate of random, neutral changes in the genome. Non-synonymous changes, on the other hand, do change the amino acid sequence of the resulting protein, and are presumed to be more likely to have some kind of effect on the phenotype. The ratio of nonsynonymous to synonymous nucleotide changes within a gene, dN/dS, is a measure of the history of selection for change in that gene. High dN/dS values mean there has been selection pressure for novel forms, while low dN/dS values mean selection has been working to conserve the sequence.

Why pressure on cancer supression and sperm production? The former makes sense (to me at least) since we live longer than chimps and the longer lifespan seems to be adaptive. The latter? Well most of the mutations involve cell death (apatosis) in sperm, and (if I understand correctly) this just seems to be a place where there is in general a lot of selective pressue. PZ again

Mutations that help sperm escape the apoptotic culling are selectively favored, and many of the cell-death genes that are high on this list are associated with sperm cell death. In addition, changes in sperm proteins can confer advantages in sperm competition and sex conflict, and can be involved in selection for reproductive isolation.

So where is the selection for our big big brains? A commenter notes that this study only looks at the coding regions and not regulatory regions. Here is the explanation from the study authors (Neilson, et al.)

The causes for the cognitive differences may instead be sought in adaptive changes in just a few genes, in changes in gene expression, or in changes in copy number and/or organization of genes relating to cognitive function.

I'm not sure if "changes in gene expression" count as epigenetic inheritance, but it would be an incredible blow to gene-centered research if epigenetic inheritance were responsible for a good deal of our brain size.

On a related note, one of the genes subject to heavily divergent selection is SCML1. Myers notes,

Also amusingly, the name is short for "Sex Comb on Mid Leg". We have neither sex combs nor midlegs, but we've inherited this gene from our common ancestor with Drosophila.

Shouldn't this sort of thing put a damper on "gene for" talk?

I'm going to at least skim the PLoS article later today, and check out Carl Zimmer on the subject

oh yes, and hooray for the Public Library of Science!