Rad9/53BP1 protects stalled replication forks from degradation in Mec1/ATR-defective cells
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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.
Originalsprog | Engelsk |
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Tidsskrift | EMBO Reports |
Vol/bind | 19 |
Udgave nummer | 2 |
Sider (fra-til) | 351-367 |
Antal sider | 17 |
ISSN | 1469-221X |
DOI | |
Status | Udgivet - 2018 |
Eksternt udgivet | Ja |
ID: 241940552