ArticleCurrent biology : CB2010
Mad2 prolongs DNA damage checkpoint arrest caused by a double-strand break via a centromere-dependent mechanism.
Article in Current biology : CB, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 91 citations in OpenAlex.
- The Role of Arp2/3 in End-Resection During DNA Double-Strand Break Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Rewiring mitotic checkpoint control via Mps1 inhibition overcomes DNA repair-mediated resistance in glioblastoma.The Journal of biological chemistry · 2026Article
- Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints.Nature communications · 2025Article
- Arp2/3 and type-I myosins control chromosome mobility and end-resection at double-strand breaks in S. cerevisiae.Nature communications · 2025Article
- The Mediator Kinase Module regulates cell cycle re-entry and transcriptional responses following DNA damage.bioRxiv : the preprint server for biology · 2025Article
- Article
- Prolonged Cell Cycle Arrest in Response to DNA damage in Yeast Requires the Maintenance of DNA Damage Signaling and the Spindle Assembly Checkpoint.bioRxiv : the preprint server for biology · 2024Article
- Evidence of 14-3-3 proteins contributing to kinetochore integrity and chromosome congression during mitosis.Journal of cell science · 2024Article
- The increase in cell death rates in caloric restricted cells of the yeast helicase mutant rrm3 is Sir complex dependent.Scientific reports · 2023Article
- Hornerin mediates phosphorylation of the polo-box domain in Plk1 by Chk1 to induce death in mitosis.Cell death and differentiation · 2023Article
- Phosphorylation of MAD2 at Ser195 Promotes Spindle Checkpoint Defects and Sensitizes Cancer Cells to Radiotherapy in ATM Deficient Cells.Frontiers in cell and developmental biology · 2022Article
- Coupling DNA Replication and Spindle Function inCells · 2021Review
- Thymidine decreases the DNA damage and apoptosis caused by tumor-treating fields in cancer cell lines.Genes & genomics · 2021Article
- Cell-cycle phospho-regulation of the kinetochore.Current genetics · 2021Review
- Modified chromosome structure caused by phosphomimetic H2A modulates the DNA damage response by increasing chromatin mobility in yeast.Journal of cell science · 2021Article
- Complex roles of the actin-binding protein Girdin/GIV in DNA damage-induced apoptosis of cancer cells.Cancer science · 2020Article
- Yeast ATM and ATR kinases use different mechanisms to spread histone H2A phosphorylation around a DNA double-strand break.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Kinetochore protein MAD1 participates in the DNA damage response through ataxia-telangiectasia mutated kinase-mediated phosphorylation and enhanced interaction with KU80.Cancer biology & medicine · 2020Article
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Eukaryotic cells employ a suite of replication and mitotic checkpoints to ensure the accurate transmission of their DNA. In budding yeast, both the DNA damage checkpoint and the spindle assembly checkpoint (SAC) block cells prior to anaphase. The presence of a single unrepaired double-strand break (DSB) activates ATR and ATM protein kinase homologs Mec1 and Tel1, which then activate downstream effectors to trigger G2/M arrest and also phosphorylate histone H2A (creating gamma-H2AX) in chromatin surrounding the DSB. The SAC monitors proper attachment of spindle microtubules to the kinetochore formed at each centromere and the biorientation of sister centromeres toward opposite spindle pole bodies. Although these two checkpoints sense quite different perturbations, recent evidence has demonstrated both synergistic interactions and cross-talk between them. Here we report that Mad2 and other SAC proteins play an unexpected role in prolonging G2/M arrest after induction of a single DSB. This function of the SAC depends not only on Mec1 and other components of the DNA damage checkpoint but also on the presence of the centromere located > or = 90 kb from the DNA damage. DNA damage induces epigenetic changes at the centromere, including the gamma-H2AX modification, that appear to alter kinetochore function, thus triggering the canonical SAC. Thus, a single DSB triggers a response by both checkpoints to prevent the segregation of a damaged chromosome.
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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.