DNA End Resection:Facts and Mechanisms
- Author:
Liu TING
1
;
Huang Jun A
;
B
Author Information
1. Department of Cell Biology and Program in Molecular Cell Biology
- Keywords:
DNA end resection;
Homologous recombination;
DNA double-strand breaks;
Chromatin remodeling factors;
Genome stability
- From:
Genomics, Proteomics & Bioinformatics
2016;14(3):126-130
- CountryChina
- Language:Chinese
-
Abstract:
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 30 single-stranded DNA (ssDNA) tail that can invade the homologous DNA strand. The generation of 30 ssDNA is not only essential for HR repair, but also promotes activation of the ataxia telangiectasia and Rad3-related protein (ATR). Multiple fac-tors, 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.
