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RAD51C deficiency in mice results in early prophase I arrest in males and sister chromatid separation at metaphase II in females.

  • Author(s): Kuznetsov, Sergey
  • Pellegrini, Manuela
  • Shuda, Kristy
  • Fernandez-Capetillo, Oscar
  • Liu, Yilun
  • Martin, Betty K
  • Burkett, Sandra
  • Southon, Eileen
  • Pati, Debananda
  • Tessarollo, Lino
  • West, Stephen C
  • Donovan, Peter J
  • Nussenzweig, Andre
  • Sharan, Shyam K
  • et al.
Abstract

RAD51C is a member of the RecA/RAD51 protein family, which is known to play an important role in DNA repair by homologous recombination. In mice, it is essential for viability. Therefore, we have generated a hypomorphic allele of Rad51c in addition to a null allele. A subset of mice expressing the hypomorphic allele is infertile. This infertility is caused by sexually dimorphic defects in meiotic recombination, revealing its two distinct functions. Spermatocytes undergo a developmental arrest during the early stages of meiotic prophase I, providing evidence for the role of RAD51C in early stages of RAD51-mediated recombination. In contrast, oocytes can progress normally to metaphase I after superovulation but display precocious separation of sister chromatids, aneuploidy, and broken chromosomes at metaphase II. These defects suggest a possible late role of RAD51C in meiotic recombination. Based on the marked reduction in Holliday junction (HJ) resolution activity in Rad51c-null mouse embryonic fibroblasts, we propose that this late function may be associated with HJ resolution.

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