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Título: | A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination |
Autor: | Muñoz-Galván, Sandra CSIC ORCID ; García-Rubio, María L. CSIC ORCID; Ortega, Pedro CSIC ORCID; Ruiz, José F. CSIC ORCID; Jimeno, Sonia CSIC; Pardo, Benjamín CSIC ORCID; Gómez-González, Belén CSIC ORCID; Aguilera, Andrés CSIC ORCID | Fecha de publicación: | 2017 | Editor: | Public Library of Science | Citación: | PLoS Genetics 13(5): e1006781 (2017) | Resumen: | Replication 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. | Versión del editor: | https://doi.org/10.1371/journal.pgen.1006781 | URI: | http://hdl.handle.net/10261/165417 | DOI: | 10.1371/journal.pgen.1006781 | Identificadores: | doi: 10.1371/journal.pgen.1006781 e-issn: 1553-7404 issn: 1553-7390 |
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Rrm3break.pdf | 6,64 MB | Adobe PDF | Visualizar/Abrir |
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