Distinct roles of RECQL5 in RAD51-mediated fork reversal and transcription elongation.

ABSTRACT: RECQL5 helicase has been implicated in the regulation of homologous recombination (HR), replication stress responses, transcription elongation, and resolution of transcription-replication conflicts. However, the underlying mechanism by which RECQL5 regulates multiple functions in genome maintenance is obscure. Here, we find that RECQL5 localizes to the stalled fork sites and restricts RAD51-mediated excessive fork reversal to promote unrestrained DNA synthesis. The replication defect in the absence of RECQL5 can be rescued by co-depletion of SMARCAL1/ZRANB3/HLTF/FBH1 fork remodelers and expression of HR-defective mutants of RAD51. The RAD51 regulation at the stalled fork sites by RECQL5 requires its binding to PCNA, RAD51, and helicase activity and is independent of its interaction with RN

SUBMITTER: Nagraj T 

PROVIDER: S-EPMC12526125 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature