Replicated chromatin curtails 53BP1 recruitment in BRCA1-proficient and BRCA1-deficient cells.

ABSTRACT: DNA double-strand breaks can be repaired by non-homologous end-joining or homologous recombination. Which pathway is used depends on the balance between the tumor suppressors 53BP1 and BRCA1 and on the availability of an undamaged template DNA for homology-directed repair. How cells switch from a 53BP1-dominated to a BRCA1-governed homologous recombination response as they progress through the cell cycle is incompletely understood. Here we reveal, using high-throughput microscopy and applying single cell normalization to control for increased genome size as cells replicate their DNA, that 53BP1 recruitment to damaged replicated chromatin is inefficient in both BRCA1-proficient and BRCA1-deficient cells. Our results substantiate a dual switch model from a 53BP1-dominated response in unrepli

SUBMITTER: Michelena J 

PROVIDER: S-EPMC8046418 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature