DNA End Resection: Facts and

Genomics, Proteomics & Bioinformatics

Ting Liu¹  Jun Huang² 

[1] Department of Cell Biology and Program in Molecular Cell Biology, Zhejiang University School of Medicine, Hangzhou 310058, China;Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China;

关键词: DNA end resection;    Homologous recombination;    DNA double-strand breaks;    Chromatin remodeling factors;    Genome stability;   

DOI  :  10.1016/j.gpb.2016.05.002

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown