ArticlePLoS genetics2011
Sensing of replication stress and Mec1 activation act through two independent pathways involving the 9-1-1 complex and DNA polymerase ε.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Dpb11 facilitates the colocalization of Mec1-Ddc2 with its activators on gapped DNA.Cell reports · 2026Article
- Molecular interplay between the DNA damage checkpoint kinase Mec1-Ddc2 and its activator Dpb11 on gapped DNA.bioRxiv : the preprint server for biology · 2025Article
- The loss of DNA polymerase epsilon accessory subunits POLE3-POLE4 leads to BRCA1-independent PARP inhibitor sensitivity.Nucleic acids research · 2024Article
- Transcription as source of genetic heterogeneity in budding yeast.Yeast (Chichester, England) · 2024Review
- Replication stress response defects are associated with response to immune checkpoint blockade in nonhypermutated cancers.Science translational medicine · 2021Article
- Dpb4 promotes resection of DNA double-strand breaks and checkpoint activation by acting in two different protein complexes.Nature communications · 2021Article
- Mechanism of auto-inhibition and activation of Mec1Nature structural & molecular biology · 2021Article
- Rad9, a 53BP1 Ortholog of Budding Yeast, Is Insensitive to Spo11-Induced Double-Strand Breaks During Meiosis.Frontiers in cell and developmental biology · 2021Article
- Cohesin Causes Replicative DNA Damage by Trapping DNA Topological Stress.Molecular cell · 2020Article
- Plant DNA Polymerases.International journal of molecular sciences · 2019Review
- RNase H activities counteract a toxic effect of Polymerase η in cells replicating with depleted dNTP pools.Nucleic acids research · 2019Article
- Phosphorylation of Histone H4T80 Triggers DNA Damage Checkpoint Recovery.Molecular cell · 2018Article
- Genetic Evidence for Roles of Yeast Mitotic Cyclins at Single-Stranded Gaps Created by DNA Replication.G3 (Bethesda, Md.) · 2018Article
- S-phase checkpoint regulations that preserve replication and chromosome integrity upon dNTP depletion.Cellular and molecular life sciences : CMLS · 2017Review
- Function of the Plant DNA Polymerase Epsilon in Replicative Stress Sensing, a Genetic Analysis.Plant physiology · 2017Article
- Mutations in the Non-Catalytic Subunit Dpb2 of DNA Polymerase Epsilon Affect the Nrm1 Branch of the DNA Replication Checkpoint.PLoS genetics · 2017Article
- Role of the Polymerase ϵ sub-unit DPB2 in DNA replication, cell cycle regulation and DNA damage response in Arabidopsis.Nucleic acids research · 2016Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- A conserved Polϵ binding module in Ctf18-RFC is required for S-phase checkpoint activation downstream of Mec1.Nucleic acids research · 2015Article
- Assembly of Slx4 signaling complexes behind DNA replication forks.The EMBO journal · 2015Article
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4 authors.
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Abstract
Following DNA damage or replication stress, budding yeast cells activate the Rad53 checkpoint kinase, promoting genome stability in these challenging conditions. The DNA damage and replication checkpoint pathways are partially overlapping, sharing several factors, but are also differentiated at various levels. The upstream kinase Mec1 is required to activate both signaling cascades together with the 9-1-1 PCNA-like complex and the Dpb11 (hTopBP1) protein. After DNA damage, Dpb11 is also needed to recruit the adaptor protein Rad9 (h53BP1). Here we analyzed the mechanisms leading to Mec1 activation in vivo after DNA damage and replication stress. We found that a ddc1Δdpb11-1 double mutant strain displays a synthetic defect in Rad53 and H2A phosphorylation and is extremely sensitive to hydroxyurea (HU), indicating that Dpb11 and the 9-1-1 complex independently promote Mec1 activation. A similar phenotype is observed when both the 9-1-1 complex and the Dpb4 non-essential subunit of DNA polymerase ε (Polε) are contemporarily absent, indicating that checkpoint activation in response to replication stress is achieved through two independent pathways, requiring the 9-1-1 complex and Polε.
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