ArticleGenetics2010
The fission yeast Rad32(Mre11)-Rad50-Nbs1 complex acts both upstream and downstream of checkpoint signaling in the S-phase DNA damage checkpoint.
Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Analyzing DNA Replication Fork Stability and Collapse Using Chromatin Fiber Analysis and the R-ODD-BLOBS Program.Computational and structural biotechnology journal · 2026Article
- Modelling DNA replication fork stability and collapse using chromatin fiber analysis and the R-ODD-BLOBS program.bioRxiv : the preprint server for biology · 2025Article
- DNA Repair Cofactors ATMIN and NBS1 Are Required to Suppress T Cell Activation.PLoS genetics · 2015Article
- Initiation of DNA damage responses through XPG-related nucleases.The EMBO journal · 2013Article
- Role for the mammalian Swi5-Sfr1 complex in DNA strand break repair through homologous recombination.PLoS genetics · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Mre11-Rad50-Nbs1 (MRN) heterotrimer plays various and complex roles in DNA damage repair and checkpoint signaling. Its role in activating Ataxia-Telangiectasia Mutated (ATM), the central checkpoint kinase in the metazoan double-strand break response, has been well studied. However, its function in the checkpoint independent of ATM activation, as well as functions that are completely checkpoint independent, are less well understood. In fission yeast, DNA damage checkpoint signaling requires Rad3, the homolog of the ATR (ATM and Rad3-related) kinase, not Tel1, the ATM homolog, allowing us to dissect MRN's ATM-independent S-phase DNA damage checkpoint roles from its role in ATM activation. We find that MRN is involved in Rad3 (ATR)-dependent checkpoint signaling in S phase, but not G2, suggesting that MRN is involved in ATR activation through its role in replication fork metabolism. In addition, we define a role for MRN in the S-phase DNA damage checkpoint-dependent slowing of replication that is independent of its role in checkpoint signaling. Genetic interactions between MRN and Rhp51, the fission yeast Rad51 homolog, lead us to suggest that MRN participates in checkpoint-dependent replication slowing through negative regulation of recombination.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.