Muñoz-Galván, SandraGarcía-Rubio, MaríaOrtega, PedroRuiz, Jose FJimeno, SoniaPardo, BenjaminGómez-González, BelénAguilera, Andrés2023-01-252023-01-252017-05-05http://hdl.handle.net/10668/11174Replication 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.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/ChromatidsDNA Breaks, Double-StrandedDNA HelicasesDNA RepairDNA ReplicationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSister Chromatid Exchangeresearch article28475600open access10.1371/journal.pgen.10067811553-7404PMC5438189https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1006781&type=printablehttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438189/pdf