Gene Duplication, Gene Conversion and the Evolution of the Y Chromosome

Connallon, Tim; Clark, Andrew G.

doi:10.1534/genetics.110.116756

Cited by 56 publications

(59 citation statements)

References 48 publications

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“…This may allow the restoration of a mutation-free gene copy at a locus with a deleterious mutation (depicted in red) through a gene conversion with another copy of the same gene family, and has been shown to oppose Y degeneration by analytical and computer simulation methods 109,110 . A consequence of gene conversion between the arms of a palindrome is a high amount of sequence identity between repeat units.…”

Section: Primate Y Chromosome As Revealed From Genomic Studiesmentioning

confidence: 99%

Y-chromosome evolution: emerging insights into processes of Y-chromosome degeneration

2013

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The human Y chromosome is intriguing not only because it harbours the master-switch gene determining gender but also because of its unusual evolutionary trajectory. Previously an autosome, Y chromosome evolution has been characterized by massive gene decay. Recent whole-genome and transcriptome analyses of Y chromosomes in humans and other primates, in Drosophila species as well as in plants have shed light on the current gene content of the Y, its origins and its long-term fate. Comparative analysis of young and old Y chromosomes have given further insights into the evolutionary and molecular forces triggering Y degeneration and its evolutionary destiny.

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Section: Primate Y Chromosome As Revealed From Genomic Studiesmentioning

confidence: 99%

Y-chromosome evolution: emerging insights into processes of Y-chromosome degeneration

2013

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“…Recombination decouples such associations, and permits diploidy to evolve, despite the long-term fitness cost. Such interactions between ploidy and recombination have parallels in various other aspects of genome evolution, including the evolution of genomic imprinting [44], [68] and the establishment of gene duplicates [69], [70].…”

Section: Resultsmentioning

confidence: 99%

Sex-Differential Selection and the Evolution of X Inactivation Strategies

Connallon

Clark

2013

PLoS Genet

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X inactivation—the transcriptional silencing of one X chromosome copy per female somatic cell—is universal among therian mammals, yet the choice of which X to silence exhibits considerable variation among species. X inactivation strategies can range from strict paternally inherited X inactivation (PXI), which renders females haploid for all maternally inherited alleles, to unbiased random X inactivation (RXI), which equalizes expression of maternally and paternally inherited alleles in each female tissue. However, the underlying evolutionary processes that might account for this observed diversity of X inactivation strategies remain unclear. We present a theoretical population genetic analysis of X inactivation evolution and specifically consider how conditions of dominance, linkage, recombination, and sex-differential selection each influence evolutionary trajectories of X inactivation. The results indicate that a single, critical interaction between allelic dominance and sex-differential selection can select for a broad and continuous range of X inactivation strategies, including unequal rates of inactivation between maternally and paternally inherited X chromosomes. RXI is favored over complete PXI as long as alleles deleterious to female fitness are sufficiently recessive, and the criteria for RXI evolution is considerably more restrictive when fitness variation is sexually antagonistic (i.e., alleles deleterious to females are beneficial to males) relative to variation that is deleterious to both sexes. Evolutionary transitions from PXI to RXI also generally increase mean relative female fitness at the expense of decreased male fitness. These results provide a theoretical framework for predicting and interpreting the evolution of chromosome-wide expression of X-linked genes and lead to several useful predictions that could motivate future studies of allele-specific gene expression variation.

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“…Also, gene duplication coupled with gene conversion between duplicates can potentially maintain gene function by counteracting evolutionary Y decay (Rozen et al 2003;Charlesworth 2003;Noordam and Repping 2006). A combination of analytical and computer simulation methods also showed that gene conversion effectively maintains the functionality of Y-linked duplicates that have already become fixed, although it has little impact on the probability that duplicates become fixed within a population (Connallon and Clark 2010). Therefore, the functions of T. muenninki Y-linked genes may have been maintained not only by translocation but also by amplification on the sex chromosomes fused to an autosomal pair.…”

Section: Discussionmentioning

confidence: 99%

Ancestral Y-linked genes were maintained by translocation to the X and Y chromosomes fused to an autosomal pair in the Okinawa spiny rat Tokudaia muenninki

et al. 2016

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Two species of the genus Tokudaia lack the Y chromosome and SRY, but several Y-linked genes have been rescued by translocation or transposition to other chromosomes. Tokudaia muenninki is the only species in the genus that maintains the Y owing to sex chromosome-autosome fusions. According to previous studies, many SRY pseudocopies and other Y-linked genes have evolved by excess duplication in this species. Using RNA-seq and RT-PCR, we found that ZFY, EIF2S3Y, TSPY, UTY, DDX3Y, USP9Y, and RBMY, but not UBA1Y, had high deduced amino acid sequence similarity and similar expression patterns with other rodents, suggesting that these genes were functional. Based on FISH and quantitative real-time PCR, all of the genes except for UTY and DDX3Y were amplified on the X and Y chromosomes with approximately 10-66 copies in the male genome. In a comparative analysis of the 372.4-kb BAC sequence and Y-linked gene transcripts from T. muenninki with the mouse Y genomic sequence, we observed that multiple-copy genes in the ancestral Y genome were nonfunctional, indicating that the gene functions were assumed by amplified copies. We also found a LTR sequence at the distal end of a SRY duplication unit, suggesting that unequal sister chromatid exchange mediated by retrotransposable elements could have been involved in SRY amplification. Our results revealed that the Y-linked genes were rescued from degeneration via translocations to other sex chromosomal regions and amplification events in T. muenninki

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Gene Duplication, Gene Conversion and the Evolution of the Y Chromosome

Cited by 56 publications

References 48 publications

Y-chromosome evolution: emerging insights into processes of Y-chromosome degeneration

Y-chromosome evolution: emerging insights into processes of Y-chromosome degeneration

Sex-Differential Selection and the Evolution of X Inactivation Strategies

Ancestral Y-linked genes were maintained by translocation to the X and Y chromosomes fused to an autosomal pair in the Okinawa spiny rat Tokudaia muenninki

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