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.
Villa, M., Bonetti, D., Carraro, M., & Longhese, M. (2018). Rad9/53BP1 protects stalled replication forks from degradation in Mec1/ATR-defective cells. EMBO REPORTS, 19(2), 351-367 [10.15252/embr.201744910].
Citazione: | Villa, M., Bonetti, D., Carraro, M., & Longhese, M. (2018). Rad9/53BP1 protects stalled replication forks from degradation in Mec1/ATR-defective cells. EMBO REPORTS, 19(2), 351-367 [10.15252/embr.201744910]. | |
Tipo: | Articolo in rivista - Articolo scientifico | |
Carattere della pubblicazione: | Scientifica | |
Presenza di un coautore afferente ad Istituzioni straniere: | No | |
Titolo: | Rad9/53BP1 protects stalled replication forks from degradation in Mec1/ATR-defective cells | |
Autori: | Villa, M; Bonetti, D; Carraro, M; Longhese, M | |
Autori: | ||
Data di pubblicazione: | 2018 | |
Lingua: | English | |
Rivista: | EMBO REPORTS | |
Digital Object Identifier (DOI): | http://dx.doi.org/10.15252/embr.201744910 | |
Appare nelle tipologie: | 01 - Articolo su rivista |
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