RT Journal Article
T1 A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination.
A1 Muñoz-Galván, Sandra
A1 García-Rubio, María
A1 Ortega, Pedro
A1 Ruiz, Jose F
A1 Jimeno, Sonia
A1 Pardo, Benjamin
A1 Gómez-González, Belén
A1 Aguilera, Andrés
AB 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.
YR 2017
FD 2017-05-05
LK http://hdl.handle.net/10668/11174
UL http://hdl.handle.net/10668/11174
LA en
DS RISalud
RD Apr 7, 2025