ABSTRACT
Nonrecombining chromosomes, such as the Y, are expected to degenerate over time due to reduced
efficacy of natural selection compared to chromosomes that recombine. However, gene duplication,
coupled with gene conversion between duplicate pairs, can potentially counteract forces of evolutionary
decay that accompany asexual reproduction. Using a combination of analytical and computer simulation
methods, we explicitly show that, although gene conversion has little impact on the probability that
duplicates become fixed within a population, conversion can be effective at maintaining the functionality
of Y-linked duplicates that have already become fixed. The coupling of Y-linked gene duplication and
gene conversion between paralogs can also prove costly by increasing the rate of nonhomologous
crossovers between duplicate pairs. Such crossovers can generate an abnormal Y chromosome, as was
recently shown to reduce male fertility in humans. The results represent a step toward explaining some of
the more peculiar attributes of the human Y as well as preliminary Y-linked sequence data from other
mammals and Drosophila. The results may also be applicable to the recently observed pattern of
tetraploidy and gene conversion in asexual, bdelloid rotifers.
ABSTRACT
Nonrecombining chromosomes, such as the Y, are expected to degenerate over time due to reduced
efficacy of natural selection compared to chromosomes that recombine. However, gene duplication,
coupled with gene conversion between duplicate pairs, can potentially counteract forces of evolutionary
decay that accompany asexual reproduction. Using a combination of analytical and computer simulation
methods, we explicitly show that, although gene conversion has little impact on the probability that
duplicates become fixed within a population, conversion can be effective at maintaining the functionality
of Y-linked duplicates that have already become fixed. The coupling of Y-linked gene duplication and
gene conversion between paralogs can also prove costly by increasing the rate of nonhomologous
crossovers between duplicate pairs. Such crossovers can generate an abnormal Y chromosome, as was
recently shown to reduce male fertility in humans. The results represent a step toward explaining some of
the more peculiar attributes of the human Y as well as preliminary Y-linked sequence data from other
mammals and Drosophila. The results may also be applicable to the recently observed pattern of
tetraploidy and gene conversion in asexual, bdelloid rotifers.
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