RAD52-mediated repair of DNA double-stranded breaks at inactive centromeres leads to subsequent apoptotic cell death.

ABSTRACT: Centromeres, where the kinetochore complex binds, are susceptible to damages including DNA double-stranded breaks (DSBs). Here, we report the functional significance and the temporally and spatially distinct regulation of centromeric DSB repair via the three pathways of non-homologous end joining (NHEJ), homologous recombination (HR) and single-strand annealing (SSA). The SSA factor RAD52 is most frequently recruited to centromeric DSB sites compared with the HR factor RAD51 and the NHEJ factor DNA ligase IV (LIG4), indicating that SSA plays predominant roles in centromeric DSB repair. Upon centromeric DSB induction, LIG4 is recruited to both active centromeres, where kinetochore complex binds, and inactive centromeres. In contrast, RAD51 and RAD52 are recruited only to inactive centromere

SUBMITTER: Maruta G 

PROVIDER: S-EPMC11602138 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature