Rad51‐deficient vertebrate cells accumulate chromosomal breaks prior to cell death

Rad51‐deficient vertebrate cells accumulate chromosomal breaks prior to cell death Yeast rad51 mutants are viable, but extremely sensitive to γ‐rays due to defective repair of double‐strand breaks. In contrast, disruption of the murine RAD51 homologue is lethal, indicating an essential role of Rad51 in vertebrate cells. We generated clones of the chicken B lymphocyte line DT40 carrying a human RAD51 transgene under the control of a repressible promoter and subsequently disrupted the endogenous RAD51 loci. Upon inhibition of the RAD51 transgene, Rad51− cells accumulated in the G2/M phase of the cell cycle before dying. Chromosome analysis revealed that most metaphase‐arrested Rad51− cells carried isochromatid‐type breaks. In conclusion, Rad51 fulfils an essential role in the repair of spontaneously occurring chromosome breaks in proliferating cells of higher eukaryotes. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The EMBO Journal Wiley

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Publisher
Wiley
Copyright
Copyright © 2013 Wiley Periodicals, Inc
ISSN
0261-4189
eISSN
1460-2075
D.O.I.
10.1093/emboj/17.2.598
Publisher site
See Article on Publisher Site

Abstract

Yeast rad51 mutants are viable, but extremely sensitive to γ‐rays due to defective repair of double‐strand breaks. In contrast, disruption of the murine RAD51 homologue is lethal, indicating an essential role of Rad51 in vertebrate cells. We generated clones of the chicken B lymphocyte line DT40 carrying a human RAD51 transgene under the control of a repressible promoter and subsequently disrupted the endogenous RAD51 loci. Upon inhibition of the RAD51 transgene, Rad51− cells accumulated in the G2/M phase of the cell cycle before dying. Chromosome analysis revealed that most metaphase‐arrested Rad51− cells carried isochromatid‐type breaks. In conclusion, Rad51 fulfils an essential role in the repair of spontaneously occurring chromosome breaks in proliferating cells of higher eukaryotes.

Journal

The EMBO JournalWiley

Published: Jan 15, 1998

References

  • Mismatch repair‐induced meiotic recombination requires the pms1 gene product
    Borts, Borts; Leung, Leung; Kramer, Kramer; Kramer, Kramer; Williamson, Williamson; Fogel, Fogel; Haber, Haber
  • Apoptosis and programmed cell death in immunity
    Cohen, Cohen; Duke, Duke; Fadok, Fadok; Sellins, Sellins
  • Human and mouse homologs of the Saccharomyces cerevisiae RAD54 DNA repair gene: evidence for functional conservation
    Kanaar, Kanaar
  • Homologous recombination and the roles of double‐strand breaks
    Shinohara, Shinohara; Ogawa, Ogawa
  • An approximately half set of histone genes is enough for cell proliferation and a lack of several histone variants causes protein pattern changes in the DT40 chicken B cell line
    Takami, Takami; Takeda, Takeda; Nakayama, Nakayama

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