De Piccoli Giacomo, Cortes-Ledesma Felipe, Ira Gregory, Torres-Rosell Jordi, Uhle Stefan, Farmer Sarah, Hwang Ji-Young, Machin Felix, Ceschia Audrey, McAleenan Alexandra, Cordon-Preciado Violeta, Clemente-Blanco Andrés, Vilella-Mitjana Felip, Ullal Pranav, Jarmuz Adam, Leitao Beatriz, Bressan Debra, Dotiwala Farokh, Papusha Alma, Zhao Xiaolan, Myung Kyungjae, Haber James E, Aguilera Andrés, Aragón Luis
Cell Cycle Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London W12 0NN, UK.
Nat Cell Biol. 2006 Sep;8(9):1032-4. doi: 10.1038/ncb1466. Epub 2006 Aug 6.
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.
DNA双链断裂(DSB)可在DNA复制过程中产生,或在暴露于DNA损伤剂后产生,其正确修复对于细胞存活和基因组稳定性至关重要。在此,我们表明Smc5-Smc6复合物被重新招募到DSB处,以通过姐妹染色单体之间的同源重组来支持其修复。此外,我们证明Smc5-Smc6对于抑制大规模染色体重排是必需的。我们的研究结果表明,Smc5-Smc6复合物对于基因组稳定性至关重要,因为它通过无差错的姐妹染色单体重组(SCR)促进DSB的修复,从而抑制不适当的非姐妹重组事件。