RAD51 separation of function mutation maintenance but preserves DSB repair

Warning

This publication doesn't include Faculty of Economics and Administration. It includes Faculty of Medicine. Official publication website can be found on muni.cz.
Authors

SON Mi Young BELÁŇ Ondrej ŠPÍREK Mário CIBULKA Jakub NIKULENKOV Fedor KIM You Young HWANG Sunyoung MYUNG Kyungjae MONTAGNA Cristina KIM Tae Moon KREJČÍ Lumír HASTY Paul

Year of publication 2024
Type Article in Periodical
Magazine / Source iScience
MU Faculty or unit

Faculty of Medicine

Citation
web https://doi.org/10.1016/j.isci.2024.109524
Doi http://dx.doi.org/10.1016/j.isci.2024.109524
Keywords Properties of biomolecules; Genetics; Molecular biology; Molecular interaction
Description Homologous recombination (HR) protects replication forks (RFs) and repairs DNA double-strand breaks (DSBs). Within HR, BRCA2 regulates RAD51 via two interaction regions: the BRC repeats to form filaments on single-stranded DNA and exon 27 (Ex27) to stabilize the filament. Here, we identified a RAD51 S181P mutant that selectively disrupted the RAD51-Ex27 association while maintaining interaction with BRC repeat and proficiently forming filaments capable of DNA binding and strand invasion. Interestingly, RAD51 S181P was defective for RF protection/restart but proficient for DSB repair. Our data suggest that Ex27-mediated stabilization of RAD51 filaments is required for the protection of RFs, while it seems dispensable for the repair of DSBs.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.