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A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination

AuthorsMuñoz-Galván, Sandra ; García-Rubio, María L. ; Ortega, Pedro; Ruiz, José F. ; Jimeno, Sonia ; Pardo, Benjamín ; Gómez-González, Belén ; Aguilera, Andrés
Issue Date2017
PublisherPublic Library of Science
CitationPLoS Genetics 13(5): e1006781 (2017)
AbstractReplication forks stall at different DNA obstacles such as those originated by transcription. Fork stalling can lead to DNA double-strand breaks (DSBs) that will be preferentially repaired by homologous recombination when the sister chromatid is available. The Rrm3 helicase is a replisome component that promotes replication upon fork stalling, accumulates at highly transcribed regions and prevents not only transcription-induced replication fork stalling but also transcription-associated hyper-recombination. This led us to explore the possible role of Rrm3 in the repair of DSBs when originating at the passage of the replication fork. Using a mini-HO system that induces mainly single-stranded DNA breaks, we show that rrm3Δ cells are defective in DSB repair. The defect is clearly seen in sister chromatid recombination, the major repair pathway of replication-born DSBs. Our results indicate that Rrm3 recruitment to replication-born DSBs is crucial for viability, uncovering a new role for Rrm3 in the repair of broken replication forks.
Publisher version (URL)https://doi.org/10.1371/journal.pgen.1006781
Identifiersdoi: 10.1371/journal.pgen.1006781
e-issn: 1553-7404
issn: 1553-7390
Appears in Collections:(CABIMER) Artículos
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