作者: Ismail Abdou , Guy G. Poirier , Michael J. Hendzel , Michael Weinfeld
DOI: 10.1093/NAR/GKU1307
关键词:
摘要: In the current model of DNA SSBR, PARP1 is regarded as sensor single-strand breaks (SSBs). However, biochemical studies have implicated LIG3 another possible SSB sensor. Using a laser micro-irradiation protocol that predominantly generates SSBs, we were able to demonstrate dispensable for accumulation different break repair (SSBR) proteins at sites damage in live cells. Furthermore, show cells first time plays role mediating SSBR XRCC1 and PNKP damage. Importantly, did not require BRCT domain-mediated interaction with XRCC1. We N-terminal ZnF domain key enzyme's sensing function. Finally, provide cellular evidence acts caused by topoisomerase I inhibitor, irinotecan. Our results support existence second damage-sensing mechanism involving detection nicks genome LIG3.