期刊
MOLECULAR CELL
卷 73, 期 5, 页码 900-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2019.01.001
关键词
-
资金
- Canadian Cancer Society Impact grant [702310]
- Natural Sciences and Engineering Research Council of Canada PGS-D award
- Ontario Graduate Scholarship
- Italian Association for Cancer Research [AIRC IG 18976]
- Natural Sciences and Engineering Research Council of Canada Discovery grant [RGPIN-2017-06743]
Post-replication repair (PRR) allows tolerance of chemical- and UV-induced DNA base lesions in both an error-free and an error-prone manner. In classical PRR, PCNA monoubiquitination recruits translesion synthesis (TLS) DNA polymerases that can replicate through lesions. We find that PRR responds to DNA replication stress that does not cause base lesions. Rad5 forms nuclear foci during normal S phase and after exposure to types of replication stress where DNA base lesions are likely absent. Rad5 binds to the sites of stressed DNA replication forks, where it recruits TLS polymerases to repair single-stranded DNA (ssDNA) gaps, preventing mitotic defects and chromosome breaks. In contrast to the prevailing view of PRR, our data indicate that Rad5 promotes both mutagenic and error-free repair of undamaged ssDNA that arises during physiological and exogenous replication stress.
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