Melissa Wilson Sayres seminar - Sex chromosome evolution

Post date: Nov 8, 2016 12:50:03 AM

Melissa Wilson Sayres gave a very interesting talk today about sex chromosome evolution in UCLA’s Human Genetics seminar series. In her introduction, she mentioned that while mammalian Y chromosomes are much smaller than the X chromosome, this isn’t a universal feature of Y chromosomes, as the papaya Y chromosome is actually larger than the X. This struck me as really interesting! What does this tell us about Y chromosome evolution?

As background, the reason the Y chromosome is thought to be smaller than the X is that clonal inheritance of the Y means recombination can't act to remove harmful mutations. So while we started with a Y chromosome that was mostly identical to the X, over time deletions accumulated to give us our tiny Y. But deletions aren’t the only form of mutation that clonal inheritance permits. Insertions, such as transposon insertions, should also profit, which apparently has led to the large papaya Y. Why has the balance been so biased towards deletion for the mammalian Y?

My first thought was that there could be a selective advantage for smaller Y chromosomes - perhaps sperm with a small Y would be less heavy, and thus could swim faster to inseminate eggs. But it turns out that birds, in which female are the heterogametic sex, also have a tiny W chromosome (their female equivalant of the Y). So that theory doesn’t really hold up (leaving aside the question of whether a smaller Y really makes sperm that much lighter) (Hat tip to Alejandro Burga).

So now I’m thinking that maybe this has to do with the evolution of dosage compensation. Dosage compensation exists to ensure that genes on the X have similar expression levels in both sexes, despite being in one copy in XY males and two copies in XX females. Early in the evolution of sex chromosomes, dosage compensation doesn’t exist. Once recombination is lost and genes on the Y start accumulating loss-of-function mutations, chromosome-wide dosage compensation is eventually necessitated. In mammals, this works through reducing female X chromosome gene expression by half. However, at the time that dosage compensation comes into existence, perhaps there are still functional X-like genes on the degraded Y. For these genes, expression will be twice as high in XY males compared to XX females. What’s the fastest way to fix this problem? Large deletions.

In any case, I don’t know if this is already well understood, but it was fun to think about, and a fun talk! I’d love to hear the thoughts of any sex chromosome evolution experts out there.