Journal
NATURE CELL BIOLOGY
Volume 8, Issue 9, Pages 1032-U118Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb1466
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Funding
- 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
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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.
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