4.8 Article

Sexual dimorphism in the meiotic requirement for PRDM9: A mammalian evolutionary safeguard

Journal

SCIENCE ADVANCES
Volume 6, Issue 43, Pages -

Publisher

AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abb6606

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Funding

  1. JAX Scholar award [19042802-15-3]
  2. NICHD T32 Training Program in Developmental Genetics [T32 HD007065]
  3. NIH [P01 GM99640, R01 HD093778, R01 GM125736, P30 CA034196]

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In many mammals, genomic sites for recombination are determined by the histone methyltransferase PRMD9. Some mouse strains lacking PRDM9 are infertile, but instances of fertility or semifertility in the absence of PRDM9 have been reported in mice, canines, and a human female. Such findings raise the question of how the loss of PRDM9 is circumvented to maintain fertility. We show that genetic background and sex-specific modifiers can obviate the requirement for PRDM9 in mice. Specifically, the meiotic DNA damage checkpoint protein CHK2 acts as a modifier allowing female-specific fertility in the absence of PRDM9. We also report that, in the absence of PRDM9, a PRDM9-independent recombination system is compatible with female meiosis and fertility, suggesting sex-specific regulation of meiotic recombination, a finding with implications for speciation.

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