The ubiquitin protease Ubp10 suppresses the formation of translocations at Cdc13 binding sites.

ABSTRACT: Double strand breaks (DSBs) pose a significant threat to chromosome stability and, if left unrepaired, can result in chromosome rearrangements. Canonical DNA repair pathways mitigate these risks. However, if these repair mechanisms fail to repair the DSB, alternative repair pathways, such as break-induced replication (BIR), single-strand annealing (SSA), and de novo telomere addition (dnTA), can be utilized. Yeast subtelomeric regions are hotspots of recombination, while interstitial telomere-like sites can promote dnTA. In yeast, dnTA sites, termed SiRTAs (Sites of Repair-associated Telomere Addition), require Cdc13 association. We identified the ubiquitin protease Ubp10 as a positive regulator of dnTA at SiRTAs. Loss of UBP10 reduces dnTA

SUBMITTER: Gonzalez DI 

PROVIDER: S-EPMC12262540 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature