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M-phase chromosomes are also resected in cell-free extracts and cultured human cells. In contrast to the events in S phase, M-phase resection is solely dependent on MRN-CtIP. Despite generation of RPA-ssDNA, M-phase resection does not lead to ATR activation or Rad51 chromatin association. Remarkably, we find that Cdk1 permits resection by phosphorylation of CtIP but also prevents Rad51 binding to the resected ends. We have thus identified Cdk1 as a critical regulator of DSB repair in M phase. Cdk1 induces persistent ssDNA-RPA overhangs in M phase, thereby preventing both classical NHEJ and Rad51-dependent HDR.<\/jats:p>","DOI":"10.1083\/jcb.201103103","type":"journal-article","created":{"date-parts":[[2011,9,5]],"date-time":"2011-09-05T15:44:59Z","timestamp":1315237499000},"page":"705-720","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":77,"title":["Cdk1 uncouples CtIP-dependent resection and Rad51 filament formation during M-phase double-strand break repair"],"prefix":"10.1083","volume":"194","author":[{"given":"Shaun E.","family":"Peterson","sequence":"first","affiliation":[{"name":"Institute for Cancer Genetics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Biological Sciences 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Genetics and Development 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Institute of Cancer Research 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Biochemistry and Molecular Biophysics 1 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