Document Type
Article
Publication Date
February 2007
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.
Recommended Citation
Kuznetsov, Sergey; Pellegrini, Manuela; Shuda, Kristy; Fernandez-Capetillo, Oscar ; Liu, Yilun; Martin, Betty K.; Burkett, Sandra; Southon, Eileen; Pati, Debananda; Tessarollo, Lino; West, Stephen D.; Donovan, Peter J.; Nussenzweig, Andre ; and Sharan, Shyam K., "RAD51C deficiency in mice results in early prophase I arrest in males and sister chromatid separation at metaphase II in females" (2007). Department of Biochemistry and Molecular Biology Faculty Papers. Paper 10.
https://jdc.jefferson.edu/bmpfp/10
Comments
This article has been peer reviewed. It was published in The Journal of Cell Biology 176(5):581-592, February 2007, available at http://dx.doi.org/10.1083/jcb.200608130. Copyright by The Rockefeller University Press.