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本文引用的文献

1
Nonhomologous end joining in yeast.酵母中的非同源末端连接
Annu Rev Genet. 2005;39:431-51. doi: 10.1146/annurev.genet.39.073003.113340.
2
SMC5 and SMC6 genes are required for the segregation of repetitive chromosome regions.SMC5和SMC6基因是重复染色体区域分离所必需的。
Nat Cell Biol. 2005 Apr;7(4):412-9. doi: 10.1038/ncb1239. Epub 2005 Mar 27.
3
Postreplicative recruitment of cohesin to double-strand breaks is required for DNA repair.DNA修复需要复制后将黏连蛋白招募到双链断裂处。
Mol Cell. 2004 Dec 22;16(6):1003-15. doi: 10.1016/j.molcel.2004.11.026.
4
DNA damage response pathway uses histone modification to assemble a double-strand break-specific cohesin domain.DNA损伤反应途径利用组蛋白修饰来组装一个双链断裂特异性黏连蛋白结构域。
Mol Cell. 2004 Dec 22;16(6):991-1002. doi: 10.1016/j.molcel.2004.11.027.
5
Equal sister chromatid exchange is a major mechanism of double-strand break repair in yeast.均等姐妹染色单体交换是酵母中双链断裂修复的主要机制。
Mol Cell. 2003 Jun;11(6):1661-71. doi: 10.1016/s1097-2765(03)00183-7.
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NEJ1 controls non-homologous end joining in Saccharomyces cerevisiae.NEJ1在酿酒酵母中控制非同源末端连接。
Nature. 2001 Dec 6;414(6864):666-9. doi: 10.1038/414666a.
7
Sister chromatid cohesion is required for postreplicative double-strand break repair in Saccharomyces cerevisiae.在酿酒酵母中,姐妹染色单体黏连对于复制后双链断裂修复是必需的。
Curr Biol. 2001 Jun 26;11(12):991-5. doi: 10.1016/s0960-9822(01)00271-8.
8
SGS1, the Saccharomyces cerevisiae homologue of BLM and WRN, suppresses genome instability and homeologous recombination.SGS1是BLM和WRN在酿酒酵母中的同源物,可抑制基因组不稳定性和同源重组。
Nat Genet. 2001 Jan;27(1):113-6. doi: 10.1038/83673.
9
Multiple pathways of recombination induced by double-strand breaks in Saccharomyces cerevisiae.酿酒酵母中双链断裂诱导的多种重组途径。
Microbiol Mol Biol Rev. 1999 Jun;63(2):349-404. doi: 10.1128/MMBR.63.2.349-404.1999.
10
Double-strand break repair in yeast requires both leading and lagging strand DNA polymerases.酵母中的双链断裂修复需要前导链和后随链DNA聚合酶。
Cell. 1999 Feb 5;96(3):415-24. doi: 10.1016/s0092-8674(00)80554-1.

Smc5-Smc6通过促进姐妹染色单体重组来介导DNA双链断裂修复。

Smc5-Smc6 mediate DNA double-strand-break repair by promoting sister-chromatid recombination.

作者信息

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

机构信息

Cell Cycle Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London W12 0NN, UK.

出版信息

Nat Cell Biol. 2006 Sep;8(9):1032-4. doi: 10.1038/ncb1466. Epub 2006 Aug 6.

DOI:10.1038/ncb1466
PMID:16892052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4493748/
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.

摘要

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。