HELQ is a dual-function DSB repair enzyme modulated by RPA and RAD51.

ABSTRACT: DNA double-stranded breaks (DSBs) are deleterious lesions, and their incorrect repair can drive cancer development¹. HELQ is a superfamily 2 helicase with 3' to 5' polarity, and its disruption in mice confers germ cells loss, infertility and increased predisposition to ovarian and pituitary tumours^2-4. At the cellular level, defects in HELQ result in hypersensitivity to cisplatin and mitomycin C, and persistence of RAD51 foci after DNA damage^3,5. Notably, HELQ binds to RPA and the RAD51-paralogue BCDX2 complex, but the relevance of these interactions and how HELQ functions in DSB repair remains unclear^3,5,6. Here we show that HELQ helicase activity and a previously unappreciated DNA strand annealing function are differentially regulated by RPA an

SUBMITTER: Anand R 

PROVIDER: S-EPMC8755542 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature