Abstract
XRCC2 protein shares weak amino acid sequence similarity with Rad51, which is a central player in homologous recombinational repair (HRR). Rad51 proteins assemble at the sites of HRR and form visible nuclear foci in response to DNA damage. Xrcc2 hamster mutant irs1 cells are incapable of forming Rad51 foci after ionizing irradiation or DNA cross-linking agent mitomycin C treatment, though the Rad51 protein level is normal in the mutant. The defect can be corrected in an XRCC2 transformant. Time course study showed that the irs1 cells primarily lacked the early response (2 hours after irradiation) to form small Rad51 foci (type 1) and later response (8 hours after irradiation) to form large foci (type 2). These results suggested that XRCC2 is essential for the assembly of the DNA damage-induced Rad51 foci and that XRCC2 may play an important role in the early stage of HRR.
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