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The Caenorhabditis elegans WRN helicase promotes double‐strand DNA break repair by mediating end resection and checkpoint activation
Author(s) -
Ryu JinSun,
Koo HyeonSook
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12724
Subject(s) - helicase , caenorhabditis elegans , microbiology and biotechnology , g2 m dna damage checkpoint , dna , chemistry , homologous recombination , biology , cell cycle checkpoint , genetics , cell cycle , gene , rna
The protein associated with Werner syndrome ( WRN ), is involved in DNA repair, checkpoint activation, and telomere maintenance. To better understand the involvement of WRN in double‐strand DNA break ( DSB ) repair, we analyzed the combinatorial role of WRN ‐1, the Caenorhabditis elegans WRN helicase, in conjunction with EXO ‐1 and DNA ‐2 nucleases. We found that WRN ‐1 cooperates with DNA ‐2 to resect DSB ends in a pathway acting in parallel to EXO ‐1. The wrn‐1 mutants show an aberrant accumulation of replication protein A ( RPA ) and RAD ‐51, and the same pattern of accumulation is also observed in checkpoint‐defective strains. We conclude that WRN ‐1 plays a conserved role in the resection of DSB ends and mediates checkpoint signaling, thereby influencing levels of RPA and RAD ‐51.