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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

  1. Author:
    Kuznetsov, S.
    Pellegrini, M.
    Shuda, K.
    Fernandez-Capetillo, O.
    Liu, Y. L.
    Martin, B. K.
    Burkett, S.
    Southon, E.
    Pati, D.
    Tessarollo, L.
    West, S. C.
    Donovan, P. J.
    Nussenzweig, A
    Sharan, S. K.

  2. Author Address

    NCI, Mouse Canc Genet Program, Canc Res Ctr, Frederick, MD 21702 USA. NCI, Expt Immunol Branch, Bethesda, MD 20892 USA. Thomas Jefferson Univ, Kimmerl Canc Ctr, Philadelphia, PA 19107 USA. Imperial Canc Res Fund, Clare Hall Labs, London Res Inst, Canc Res UK, S Mimms EN6 3LD, Herts, England. Baylor Coll Med, Dept Pediat, Texas Childrens Canc Ctr, Houston, TX 77030 USA. Johns Hopkins Univ, Inst Cell Engn, Baltimore, MD 21205 USA.;Sharan, SK, NCI, Mouse Canc Genet Program, Canc Res Ctr, Frederick, MD 21702 USA.;ssharan@mail.ncifcrf.gov
    1. Year: 2007
    2. Date: Feb
  2. Journal: Journal of Cell Biology
    1. 176
    2. 5
    3. Pages: 581-592
  4. Type of Article: Article
  5. ISSN: 0021-9525
  1. 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 RAD51mediated 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. broblasts, we propose that this late function may be associated with HJ resolution.

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  2. DOI: 10.1083/jcb.200608130
  3. View record in Web of Science®
  4. WOS: 000244487100017

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