Journal
FEBS LETTERS
Volume 591, Issue 14, Pages 2155-2166Publisher
WILEY
DOI: 10.1002/1873-3468.12724
Keywords
checkpoint activation; double-strand DNA break repair; end resection
Funding
- NIH Office of Research Infrastructure Programs [P40 OD010440]
- Basic Science Research program through the National Research Foundation of Korea (NRF) - Ministry of Education [2014R1A1A2-057049]
- NRF grant - Ministry of Education, Science and Technology of Korea [2012-029610]
- Brain Korea 21 PLUS program
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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.
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