DNA End Resection: Facts and Mechanisms | Zendy

Ting Liu | Zendy; Jun Huang | Zendy

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DNA End Resection: Facts and Mechanisms

Author(s) -

Ting Liu,

Jun Huang

Publication year - 2016

Publication title -

genomics proteomics and bioinformatics

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.114

H-Index - 49

eISSN - 2210-3244

pISSN - 1672-0229

DOI - 10.1016/j.gpb.2016.05.002

Subject(s) - helicase , homologous recombination , rad50 , exonuclease , non homologous end joining , replication protein a , chromatin , nuclease , dna , dna repair , biology , dna repair protein xrcc4 , microbiology and biotechnology , dna damage , genetics , nucleotide excision repair , dna binding protein , dna polymerase , gene , rna , transcription factor

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.

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