A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination
|Author||Muñoz Galván, Sandra
García Rubio, María Luisa
Ortega Moreno, Pedro
Ruiz Pérez, José Francisco
Jimeno González, Sonia
Gómez González, Belén
Aguilera López, Andrés
|Department||Universidad de Sevilla. Departamento de Genética|
|Published in||PLoS Genetics, 13 (5), 1-18.|
|Abstract||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 ...
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.
|Cite||Muñoz Galván, S., García Rubio, M.L., Ortega Moreno, P., Ruiz Pérez, J.F., Jimeno González, S., Pardo, B.,...,Aguilera López, A. (2017). A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination. PLoS Genetics, 13 (5), 1-18.|