期刊
EMBO JOURNAL
卷 20, 期 19, 页码 5513-5520出版社
WILEY
DOI: 10.1093/emboj/20.19.5513
关键词
DT40; homologous recombination; Rad51 paralogs; Rad52; XRCC3
Yeast Rad52 DNA-repair mutants exhibit pronounced radiation sensitivity and a defect in homologous recombination (HR), whereas vertebrate cells lacking Rad52 exhibit a nearly normal phenotype. Biochemical studies show that both yeast Rad52 and Rad55-57 (Rad51 paralogs) stimulate DNA-strand exchange mediated by Rad51. These findings raise the possibility that Rad51 paralogs may compensate for lack of Rad52 in vertebrate cells, explaining the absence of prominent phenotypes for Rad52-deficient cells. To test this hypothesis, using chicken DT40 cells, we generated conditional mutants deficient in both RAD52 and XRCC3, which is one of the five vertebrate PAD51 paralogs. Surprisingly, the rad52 xrcc3 double-mutant cells were non-viable and exhibited extensive chromosomal breaks, whereas rad52 and xrcc3 single mutants grew well. Our data reveal an overlapping (but non-reciprocal) role for Rad52 and XRCC3 in repairing DNA double-strand breaks. The present study shows that Rad52 can play an important role in HR repair by partially substituting for a Rad51 paralog.
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