期刊
NATURE CELL BIOLOGY
卷 8, 期 9, 页码 1032-U118出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb1466
关键词
-
类别
资金
- Medical Research Council [MC_U120074328] Funding Source: Medline
- NIGMS NIH HHS [R01 GM080600, R37 GM020056, GM20056, R01 GM020056] Funding Source: Medline
- Medical Research Council [MC_U120074328] Funding Source: researchfish
- MRC [MC_U120074328] Funding Source: UKRI
DNA double-strand breaks (DSB) can arise during DNA replication, or after exposure to DNA-damaging agents, and their correct repair is fundamental for cell survival and genomic stability. Here, we show that the Smc5-Smc6 complex is recruited to DSBs de novo to support their repair by homologous recombination between sister chromatids. In addition, we demonstrate that Smc5-Smc6 is necessary to suppress gross chromosomal rearrangements. Our findings show that the Smc5-Smc6 complex is essential for genome stability as it promotes repair of DSBs by error-free sisterchromatid recombination (SCR), thereby suppressing inappropriate non-sister recombination events.
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