Muller's Rachet and the Y-Chromosome

Continuing the discussion from Darwinism Falsified in Science Long Ago?:

The study I’m referencing is here:

Note, this is a fly study, but it will very likely carry over to humans.


That is very cool, but I don’t think it’s entirely fair to say that Y chromosomes have “evaded” Muller’s ratchet. The ubiquity of gene loss and transposable element accumulation is a testament to the fact that Muller’s ratchet is/has occurred. More like they’ve (at least in mammals) managed to endure, despite the fact that they’re subject to Muller’s ratchet.


I can go with this. They have certainly been subject to streamlining (like Lenski’s bacteria!), But they found a way of preventing a slide into total destruction. I always wondered about how.

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First off, it’s cool to see new sequencing technology leading to new discoveries. The acceleration of technology within in the last 20 years in the realm of scientific research has been amazing to witness.

I just wanted to make sure I have the correct understanding of what is in this article. For autosomal chromosomes, there is an extra copy of a gene which can supply a needed function if the allele on the other chromosome is non-functional. Sexual reproduction and cross-over events allows non-functional deleterious alleles to be removed from the population independently of other genes in the genome. This allows evolution to keep the good stuff while kicking out the bad stuff.

The y-chromosme can’t do this because it has no partner. Instead, there are multiple “alleles” (i.e. copies) on the same chromosome. There can’t be cross-over events between two chromosomes, but the large number of repeat elements in the y-chromosome results in a high rate of homologous recombination within the y-chromosome which effectively mimics what happens between autosomal chromosomes. If a functional gene replaces a non-functional deleterious copy of that gene then there will be positive selection for this new arrangement. Since there is a lot of repeats, there can be some independence between genes like there is in the autosomal chromosomes.

Is this correct?

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Yes, that’s right. But there are a large number of extra copies.

This also opens up a whole host of mechanisms for biasing gene conversion towards error correction. Gene conversion is not 50/50 like recombination, and this can be exploited to prevent drift away from sex determinant function. It is a system that can prevent drift at the protein coding level. Given how sex determination works, this is a brilliant solution to an important puzzle population genetics.

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