Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-017-02144-5
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Funding
- Institut Curie
- CNRS
- Fondation ARC
- Fondation Ligue (comite Essone)
- Institut National du Cancer [INCA 2013-1-PLBIO-14]
- Fondation pour la Recherche Medicale [Equipe FRM DEQ20160334889, ING20111223450, FDT20160435131]
- Institut Curie international PhD program, a French governmental fellowship
- l'Agence Nationale de la Recherche [ANR-14-CE10-0010-01]
- Agence Nationale de la Recherche (ANR) [ANR-14-CE10-0010] Funding Source: Agence Nationale de la Recherche (ANR)
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Replication requires homologous recombination (HR) to stabilize and restart terminally arrested forks. HR-mediated fork processing requires single stranded DNA (ssDNA) gaps and not necessarily double strand breaks. We used genetic and molecular assays to investigate fork-resection and restart at dysfunctional, unbroken forks in Schizosaccharomyces pombe. Here, we report that fork-resection is a two-step process regulated by the non-homologous end joining factor Ku. An initial resection mediated by MRN-Ctp1 removes Ku from terminally arrested forks, generating similar to 110 bp sized gaps obligatory for subsequent Exo1-mediated long-range resection and replication restart. The mere lack of Ku impacts the processing of arrested forks, leading to an extensive resection, a reduced recruitment of RPA and Rad51 and a slower fork-restart process. We propose that terminally arrested forks undergo fork reversal, providing a single DNA end for Ku binding. We uncover a role for Ku in regulating end-resection of unbroken forks and in fine-tuning HR-mediated replication restart.
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