ArticleThe EMBO journal2011
Dpb11 coordinates Mec1 kinase activation with cell cycle-regulated Rad9 recruitment.
Article in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
84 citing papers in PubMed, 117 citations in OpenAlex.
- Dpb11 facilitates the colocalization of Mec1-Ddc2 with its activators on gapped DNA.Cell reports · 2026Article
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- Increased replication-associated single-stranded DNA promotes formaldehyde-induced mutagenesis.bioRxiv : the preprint server for biology · 2026Article
- Slx4 and Fun30/SMARCAD1 coordinate S-phase checkpoint regulation and replication fork protection in response to Top1-DNA crosslinks.Nucleic acids research · 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
- DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025Review
- Multifaceted roles of H2B mono-ubiquitylation in D-loop metabolism during homologous recombination repair.Nucleic acids research · 2025Article
- Separable roles of the DNA damage response kinase Mec1ATR and its activator Rad24RAD17 during meiotic recombination.PLoS genetics · 2024Article
- Multi-step control of homologous recombination via Mec1/ATR suppresses chromosomal rearrangements.The EMBO journal · 2024Article
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- γH2A/γH2AX Mediates DNA Damage-Specific Control of Checkpoint Signaling inInternational journal of molecular sciences · 2024Article
- The Chromatin Landscape around DNA Double-Strand Breaks in Yeast and Its Influence on DNA Repair Pathway Choice.International journal of molecular sciences · 2023Review
- Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions.Nature communications · 2022Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- The DNA damage checkpoint: A tale from budding yeast.Frontiers in genetics · 2022Review
- Phosphorylation-dependent assembly of DNA damage response systems and the central roles of TOPBP1.DNA repair · 2021Review
- Rad9-mediated checkpoint activation is responsible for elevated expansions of GAA repeats in CST-deficient yeast.Genetics · 2021Article
- Dpb4 promotes resection of DNA double-strand breaks and checkpoint activation by acting in two different protein complexes.Nature communications · 2021Article
- Histones on fire: the effect of Dun1 and Mrc1 on origin firing and replication of hyper-acetylated genomes.Current genetics · 2021Review
- Phosphoproteomics reveals a distinctive Mec1/ATR signaling response upon DNA end hyper-resection.The EMBO journal · 2021Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Eukaryotic cells respond to DNA damage by activating checkpoint signalling pathways. Checkpoint signals are transduced by a protein kinase cascade that also requires non-kinase mediator proteins. One such mediator is the Saccharomyces cerevisiae Dpb11 protein, which binds to and activates the apical checkpoint kinase, Mec1. Here, we show that a ternary complex of Dpb11, Mec1 and another key mediator protein Rad9 is required for efficient Rad9 phosphorylation by Mec1 in vitro, and for checkpoint activation in vivo. Phosphorylation of Rad9 by cyclin-dependent kinase (CDK) on two key residues generates a binding site for tandem BRCT repeats of Dpb11, and is thereby required for Rad9 recruitment into the ternary complex. Checkpoint signalling via Dpb11, therefore, does not efficiently occur during G1 phase when CDK is inactive. Thus, Dpb11 coordinates checkpoint signal transduction both temporally and spatially, ensuring the initiator kinase is specifically activated in proximity of one of its critical substrates.
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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.