Rad9/53BP1 protects stalled replication forks from degradation in Mec1/ATR-defective cells.
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.
Mesh Terms:
Cell Cycle Proteins, DNA Replication, Intracellular Signaling Peptides and Proteins, Microbial Viability, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Stress, Physiological, Tumor Suppressor p53-Binding Protein 1
Cell Cycle Proteins, DNA Replication, Intracellular Signaling Peptides and Proteins, Microbial Viability, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Stress, Physiological, Tumor Suppressor p53-Binding Protein 1
EMBO Rep.
Date: Dec. 01, 2017
PubMed ID: 29301856
View in: Pubmed Google Scholar
Download Curated Data For This Publication
215032
Switch View:
- Interactions 9