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

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. © 2017 muñoz-galván et al.