A new paper in Science (Rajiv McCoy as main author) says that there’s a genetic variant, probably in the gene PLK4, that substantially increases the fraction of embryos with screwed-up chromosomes. Mothers with the high-risk genotypes apparently have fewer embryos that survive to 5 days. And, oddly enough, the variant causing this is quite common – spread all over the world, in the 20-45% frequency range. It looks as if it’s the product of a old partial selective sweep in humans ( Neanderthals don’t seem to have had it). PLK4 regulates centriole duplication, a key component of the centrosome cycle.
So far so good – a nice piece of work. But then they try to explain it.
Their idea is that reducing fecundability was itself advantageous, because it obscured paternity. I don’t believe a word of it.
First realize that the selective cost isn’t as high as you might think: generally people could only feed a couple of kids anyhow. Taking an extra month or two to start that kid is a cost, but not as big as the fraction of embryos lost might make you think. On the other hand, there would be a big selective advantage for a genotype that was resistant to these pro-aneuploidy alleles..
I’d bet on meiotic drive. Intragenomic conflict. Not crazy for a gene involved in the centrosome: centrosome genes associated with meiotic drive have been seen in Drosophila.
If the aneuploidy allele was transmitted to, say, 54% of the offspring of a heterozygote mother, it could work.
There would of course be a net disadvantage in homozygotes, because A. the aneuploidy is worse and B. the allele is competing with itself – so winning is impossible.
With a net disadvantage in homozygotes, the sweep never reaches 100%.