The epistatic relationship between BRCA2 and the other RAD51 mediators in homologous recombination

Rad51 recombinase polymerizes at the site of double-strand breaks (dsbs) where it performs dsb repair. the loss of rad51 causes extensive chromosomal breaks,leading to apoptosis. the polymerization of rad51 is regulated by a number of rad51 mediators,such as brca1,brca2,rad52,sfr1,sws1,and the five rad51 paralogs,including xrcc3. we here show that brca2-null mutant cells were able to proliferate,indicating that rad51 can perform dsb repair in the absence of brca2. we disrupted the brca1,rad52,sfr1,sws1,and xrcc3 genes in the brca2-null cells. all the resulting double-mutant cells displayed a phenotype that was very similar to that of the brca2-null cells. we suggest that brca2 might thus serve as a platform to recruit various rad51 mediators at the appropriate position at the dna-damage site. © 2011 qing et al.