作者: Min Gao , Wei Wei , Ming-Ming Li , Yong-Sheng Wu , Zhaoqing Ba
DOI: 10.1038/CR.2014.36
关键词:
摘要: DNA double-strand breaks (DSBs) are highly cytotoxic lesions and pose a major threat to genome stability if not properly repaired. We others have previously shown that class of DSB-induced small RNAs (diRNAs) is produced from sequences around DSB sites. DiRNAs associated with Argonaute (Ago) proteins play an important role in repair, though the mechanism through which they act remains unclear. Here, we report diRNAs repair restricted by homologous recombination (HR) it specifically relies on effector protein Ago2 mammalian cells. Interestingly, show forms complex Rad51 interaction enhanced cells treated ionizing radiation. demonstrate accumulation at sites HR depend catalytic activity RNA-binding capability Ago2. In contrast, resection as well RPA Mre11 loading unaffected or Dicer depletion, suggesting very likely functions directly mediating DSBs. Taken together, our findings suggest guided diRNAs, can promote recruitment and/or retention DSBs facilitate HR.