Biochemical mechanism of DSB end resection and its regulation

James M. Daley, Hengyao Niu, Adam S. Miller, Patrick Sung

Research output: Contribution to journalArticlepeer-review

54 Scopus citations

Abstract

DNA double-strand breaks (DSBs) in cells can undergo nucleolytic degradation to generate long 3' single-stranded DNA tails. This process is termed DNA end resection, and its occurrence effectively commits to break repair via homologous recombination, which entails the acquisition of genetic information from an intact, homologous donor DNA sequence. Recent advances, prompted by the identification of the nucleases that catalyze resection, have revealed intricate layers of functional redundancy, interconnectedness, and regulation. Here, we review the current state of the field with an emphasis on the major questions that remain to be answered. Topics addressed will include how resection initiates via the introduction of an endonucleolytic incision close to the break end, the molecular mechanism of the conserved MRE11 complex in conjunction with Sae2/CtIP within such a model, the role of BRCA1 and 53BP1 in regulating resection initiation in mammalian cells, the influence of chromatin in the resection process, and potential roles of novel factors.

Original languageEnglish (US)
Pages (from-to)66-74
Number of pages9
JournalDNA Repair
Volume32
DOIs
StatePublished - Aug 1 2015
Externally publishedYes

Keywords

  • Double-strand breaks
  • Helicases
  • Nucleases
  • Recombination
  • Resection

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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