Sex chromosome-to-autosome transposition events counter Y-chromosome gene loss in mammals
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Author(s)
Hughes, Jennifer F
Skaletsky, Helen
Koutseva, Natalia
Pyntikova, Tatyana
Page, David C
Date Issued
May 2015
Journal
Genome Biology
Publisher
Biomed Central Ltd
Citation
Hughes, Jennifer F et al “Sex Chromosome-to-Autosome Transposition Events Counter Y-Chromosome Gene Loss in Mammals.” Genome Biology 16, 1 (May 2015): 104 © 2015 Hughes et al
Version
Final published version
Abstract
Background: Although the mammalian X and Y chromosomes evolved from a single pair of autosomes, they are highly differentiated: the Y chromosome is dramatically smaller than the X and has lost most of its genes. The surviving genes are a specialized set with extraordinary evolutionary longevity. Most mammalian lineages have experienced delayed, or relatively recent, loss of at least one conserved Y-linked gene. An extreme example of this phenomenon is in the Japanese spiny rat, where the Y chromosome has disappeared altogether. In this species, many Y-linked genes were rescued by transposition to new genomic locations, but until our work presented here, this has been considered an isolated case. Results: We describe eight cases of genes that have relocated to autosomes in mammalian lineages where the corresponding Y-linked gene has been lost. These gene transpositions originated from either the X or Y chromosomes, and are observed in diverse mammalian lineages: occurring at least once in marsupials, apes, and cattle, and at least twice in rodents and marmoset. For two genes - EIF1AX/Y and RPS4X/Y - transposition to autosomes occurred independently in three distinct lineages. Conclusions: Rescue of Y-linked gene loss through transposition to autosomes has previously been reported for a single isolated rodent species. However, our findings indicate that this compensatory mechanism is widespread among mammalian species. Thus, Y-linked gene loss emerges as an additional driver of gene transposition from the sex chromosomes, a phenomenon thought to be driven primarily by meiotic sex chromosome inactivation.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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Creative Commons Attribution 4.0 International License
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DOI of Published Version
https://doi.org/10.1186/S13059-015-0667-4
