Journal
EMBO REPORTS
Volume 19, Issue 2, Pages 351-367Publisher
WILEY
DOI: 10.15252/embr.201744910
Keywords
Mec1; Rad9; replication forks; resection; Sgs1
Categories
Funding
- Associazione Italiana per la Ricerca sul Cancro (AIRC) [IG 19783]
- Ministero dell'Istruzione, dell'Universita e della Ricerca (Progetti di Ricerca di Interesse Nazionale-PRIN)
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available