DNA End Resection: Facts and Mechanisms

Genomics Proteomics Bioinformatics. 2016 Jun;14(3):126-130. doi: 10.1016/j.gpb.2016.05.002. Epub 2016 May 27.

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.

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

Publication types

  • Review

MeSH terms

  • Chromatin Assembly and Disassembly
  • DNA / genetics
  • DNA / metabolism*
  • DNA Breaks, Double-Stranded*
  • DNA Repair
  • Exodeoxyribonucleases / metabolism
  • Genomic Instability
  • Homologous Recombination
  • Humans
  • RecQ Helicases / metabolism

Substances

  • DNA
  • Exodeoxyribonucleases
  • RecQ Helicases