| Literature DB >> 16892052 |
Giacomo De Piccoli1, Felipe Cortes-Ledesma, Gregory Ira, Jordi Torres-Rosell, Stefan Uhle, Sarah Farmer, Ji-Young Hwang, Felix Machin, Audrey Ceschia, Alexandra McAleenan, Violeta Cordon-Preciado, Andrés Clemente-Blanco, Felip Vilella-Mitjana, Pranav Ullal, Adam Jarmuz, Beatriz Leitao, Debra Bressan, Farokh Dotiwala, Alma Papusha, Xiaolan Zhao, Kyungjae Myung, James E Haber, Andrés Aguilera, Luis Aragón.
Abstract
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 sister-chromatid recombination (SCR), thereby suppressing inappropriate non-sister recombination events.Entities:
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Year: 2006 PMID： 16892052 PMCID： PMC4493748 DOI： 10.1038/ncb1466
Source DB: PubMed Journal: Nat Cell Biol ISSN： 1465-7392 Impact factor: 28.824