DNA End Resection: Facts and Mechanisms

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• 作者：Ting Liu¹ ; ^a ; ^{liuting518@zju.edu.cn" class="auth_mail" title="E-mail the corresponding author} ; Jun Huang² ; ^b ; ^{jhuang@zju.edu.cn" class="auth_mail" title="E-mail the corresponding author}
• 关键词：DNA end resection ; Homologous recombination ; DNA double-strand breaks ; Chromatin remodeling factors ; Genome stability
• 刊名：Genomics, Proteomics Bioinformatics
• 出版年：2016
• 出版时间：June 2016
• 年：2016
• 卷：14
• 期：3
• 页码：126-130
• 全文大小：612 K

文摘

DNA double-strand breaks (DSBs), which arise following exposure to a number of endogenous and exogenous agents, can be repaired by either the homologous recombination (HR) or non-homologous end-joining (NHEJ) pathways in eukaryotic cells. A vital step in HR repair is DNA end resection, which generates a long 3′ single-stranded DNA (ssDNA) tail that can invade the homologous DNA strand. The generation of 3′ ssDNA is not only essential for HR repair, but also promotes activation of the ataxia telangiectasia and Rad3-related protein (ATR). Multiple factors, including the MRN/X complex, C-terminal-binding protein interacting protein (CtIP)/Sae2, exonuclease 1 (EXO1), Bloom syndrome protein (BLM)/Sgs1, DNA2 nuclease/helicase, and several chromatin remodelers, cooperate to complete the process of end resection. Here we review the basic machinery involved in DNA end resection in eukaryotic cells.