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 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.
Highlights
Double-strand breaks (DSBs) are one of the most dangerous types of DNA damage because they disrupt the continuity of chromosomes [1,2]
Several chromatin remodeling factors, such as remodels the structure of chromatin (RSC), INO80, switch/sucrose non-fermentable (SWI/SNF), SWI/SNF-related matrixassociated actin-dependent regulator of chromatin subfamily A containing DEAD/H box 1 (SMARCAD1; Fun30 in yeast), and Snf2-related CREB-binding protein (CREBBP) activator protein (SRCAP; SWR1 in yeast), are involved in the process of overcoming barriers to allow repair proteins to access (Figure 1) [66,67,68,69,70,71]
homologous recombination (HR) and non-homologous end-joining (NHEJ) are the two dominant repair pathways involved in DSB repair [4,6]
Summary
Double-strand breaks (DSBs) are one of the most dangerous types of DNA damage because they disrupt the continuity of chromosomes [1,2]. DNA end resection inhibits NHEJ and triggers homology-directed DSB repair [11]. During other cell cycle phases, DNA end resection is inhibited by Ku70/80 heterodimers and other proteins; only the NHEJ pathway can be initiated [11].
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