Dataset Information


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

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 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 rrm3? 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.

SUBMITTER: Munoz-Galvan S 

PROVIDER: S-EPMC5438189 | BioStudies | 2017-01-01

REPOSITORIES: biostudies

Similar Datasets

2012-01-01 | S-EPMC3258139 | BioStudies
2013-01-01 | S-EPMC3805358 | BioStudies
2008-01-01 | S-EPMC2568021 | BioStudies
2018-01-01 | S-EPMC6126713 | BioStudies
2011-01-01 | S-EPMC3074140 | BioStudies
1000-01-01 | S-EPMC2374842 | BioStudies
2014-01-01 | S-EPMC4118467 | BioStudies
2020-01-01 | S-EPMC7673990 | BioStudies
1000-01-01 | S-EPMC3347241 | BioStudies
2019-01-01 | S-EPMC6858524 | BioStudies