Unknown

Dataset Information

0

Rad9/53BP1 protects stalled replication forks from degradation in Mec1/ATR-defective cells.


ABSTRACT: Nucleolytic processing by nucleases can be a relevant mechanism to allow repair/restart of stalled replication forks. However, nuclease action needs to be controlled to prevent overprocessing of damaged replication forks that can be detrimental to genome stability. The checkpoint protein Rad9/53BP1 is known to limit nucleolytic degradation (resection) of DNA double-strand breaks (DSBs) in both yeast and mammals. Here, we show that loss of the inhibition that Rad9 exerts on resection exacerbates the sensitivity to replication stress of Mec1/ATR-defective yeast cells by exposing stalled replication forks to Dna2-dependent degradation. This Rad9 protective function is independent of checkpoint activation and relies mainly on Rad9-Dpb11 interaction. We propose that Rad9/53BP1 supports cell viability by protecting stalled replication forks from extensive resection when the intra-S checkpoint is not fully functional.

SUBMITTER: Villa M 

PROVIDER: S-EPMC5797966 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-EPMC5879462 | biostudies-literature
| S-EPMC4931187 | biostudies-literature
| S-EPMC7809791 | biostudies-literature
| S-SCDT-EMBOJ-2019-103654 | biostudies-other
| S-EPMC3553285 | biostudies-literature
| S-EPMC7575062 | biostudies-literature
| S-EPMC5829747 | biostudies-literature
| S-EPMC2944071 | biostudies-literature
| S-EPMC10529362 | biostudies-literature
| S-EPMC9546528 | biostudies-literature