期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 25, 期 10, 页码 3934-3944出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.25.10.3934-3944.2005
关键词
-
资金
- NIEHS NIH HHS [ES12244, R01 ES012244] Funding Source: Medline
- NIGMS NIH HHS [GM071011, R01 GM071011] Funding Source: Medline
Repair of chromosome double-strand breaks (DSBs) is central to cell survival and genome integrity. Non-homologous end joining (NHEJ) is the major cellular repair pathway that eliminates chromosome DSBs. Here we report our genetic screen that identified Rsc8 and Rsc30, subunits of the Saccharomyces cerevisiae chromatin remodeling complex RSC, as novel NHEJ factors. Deletion of RSC30 gene or the C-terminal truncation of RSC8 impairs NHEJ of a chromosome DSB created by HO endonuclease in vivo. rsc30 Delta maintains a robust level of homologous recombination and the damage-induced cell cycle checkpoints. By chromatin immunoprecipitation, we show recruitment of RSC to a chromosome DSB with kinetics congruent with its involvement in NHEJ. Recruitment of RSC to a DSB depends on Mre11, Rsc30, and yKu70 proteins. Rsc1p and Rsc2p, two other RSC subunits, physically interact with yKu80p and Mre11p. The interaction of Rsc1p with Mre11p appears to be vital for survival from genotoxic stress. These results suggest that chromatin remodeling by RSC is important for NHEJ.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据