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. 1998 Jan 15;17(2):598–608. doi: 10.1093/emboj/17.2.598

Rad51-deficient vertebrate cells accumulate chromosomal breaks prior to cell death.

E Sonoda 1, M S Sasaki 1, J M Buerstedde 1, O Bezzubova 1, A Shinohara 1, H Ogawa 1, M Takata 1, Y Yamaguchi-Iwai 1, S Takeda 1
PMCID: PMC1170409  PMID: 9430650

Abstract

Yeast rad51 mutants are viable, but extremely sensitive to gamma-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.

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Selected References

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