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Sperm should evolve to make female meiosis fair

Yaniv Brandvain, Graham Coop
doi: https://doi.org/10.1101/005363
Yaniv Brandvain
1Department of Plant Biology, University of Minnesota – Twin Cities. St. Paul MN, 55108
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Graham Coop
2Center for Population Biology & Department of Evolution and Ecology University of California – Davis. Davis, CA, 95616
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Abstract

Genomic conflicts arise when an allele gains an evolutionary advantage at a cost to organismal fitness. Oögenesis is inherently susceptible to such conflicts because alleles compete to be the product of female meiosis transmitted to the egg. Alleles that distort meiosis in their favor (i.e. meiotic drivers) often decrease organismal fitness, and therefore indirectly favor the evolution of mechanisms to suppress meiotic drive. In this light, many facets of oögenesis and gametogenesis have been interpreted as mechanisms of protection against genomic outlaws. Why then is female meiosis often left uncompleted until after fertilization in many animals – potentially providing an opportunity for sperm alleles to meddle with its outcome and help like-alleles drive in heterozygous females? The population genetic theory presented herein suggests that sperm nearly always evolve to increase the fairness of female meiosis in the face of genomic conflicts. These results are consistent with current knowledge of sperm-dependent meiotic drivers (loci whose distortion of female meiosis depends on sperm genotype), and suggest that the requirement of fertilization for the completion of female meiosis potentially represents a mechanism employed by females to ensure a fair meiosis.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted May 21, 2014.
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Sperm should evolve to make female meiosis fair
Yaniv Brandvain, Graham Coop
bioRxiv 005363; doi: https://doi.org/10.1101/005363
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Sperm should evolve to make female meiosis fair
Yaniv Brandvain, Graham Coop
bioRxiv 005363; doi: https://doi.org/10.1101/005363

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