ArticleProceedings of the National Academy of Sciences of the United States of America2007
The yeast DNA damage checkpoint proteins control a cytoplasmic response to DNA damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Safeguarding genome integrity: Polo-like kinase Cdc5 and phosphatase Cdc14 orchestrate Topoisomerase II-mediated catenane resolution in mitosis.Nucleic acids research · 2026Article
- Engineering recombination machinery facilitates the construction of yeast cell factories.FEMS yeast research · 2025Review
- Nonrepair functions of DNA mismatch repair proteins: new avenues for precision oncology.Trends in cancer · 2025Review
- 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
- The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction.Genetics · 2023Article
- The vacuole shapes the nucleus and the ribosomal DNA loop during mitotic delays.Life science alliance · 2022Article
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- Help or hindrance: how do microtubule-based forces contribute to genome damage and repair?Current genetics · 2020Review
- Article
- Astral microtubule forces alter nuclear organization and inhibit DNA repair in budding yeast.Molecular biology of the cell · 2019Article
- Live cell monitoring of double strand breaks in S. cerevisiae.PLoS genetics · 2019Article
- Article
- Functions and regulation of the Polo-like kinase Cdc5 in the absence and presence of DNA damage.Current genetics · 2018Review
- Microtubule dynamics drive enhanced chromatin motion and mobilize telomeres in response to DNA damage.Molecular biology of the cell · 2017Article
- Three Different Pathways Prevent Chromosome Segregation in the Presence of DNA Damage or Replication Stress in Budding Yeast.PLoS genetics · 2015Article
- DNA Damage Response Checkpoint Activation Drives KP1019 Dependent Pre-Anaphase Cell Cycle Delay in S. cerevisiae.PloS one · 2015Article
- When genome integrity and cell cycle decisions collide: roles of polo kinases in cellular adaptation to DNA damage.Systems and synthetic biology · 2014Review
- Stopped in its tracks: negative regulation of the dynein motor by the yeast protein She1.BioEssays : news and reviews in molecular, cellular and developmental biology · 2013Article
- DNA damage checkpoint triggers autophagy to regulate the initiation of anaphase.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
A single HO endonuclease-induced double-strand break (DSB) is sufficient to activate the DNA damage checkpoint and cause Saccharomyces cells to arrest at G(2)/M for 12-14 h, after which cells adapt to the presence of the DSB and resume cell cycle progression. The checkpoint signal leading to G(2)/M arrest was previously shown to be nuclear-limited. Cells lacking ATR-like Mec1 exhibit no DSB-induced cell cycle delay; however, cells lacking Mec1's downstream protein kinase targets, Rad53 or Chk1, still have substantial G(2)/M delay, as do cells lacking securin, Pds1. This delay is eliminated only in the triple mutant chk1Delta rad53Delta pds1Delta, suggesting that Rad53 and Chk1 control targets other than the stability of securin in enforcing checkpoint-mediated cell cycle arrest. The G(2)/M arrest in rad53Delta and chk1Delta revealed a unique cytoplasmic phenotype in which there are frequent dynein-dependent excursions of the nucleus through the bud neck, without entering anaphase. Such excursions are infrequent in wild-type arrested cells, but have been observed in cells defective in mitotic exit, including the semidominant cdc5-ad mutation. We suggest that Mec1-dependent checkpoint signaling through Rad53 and Chk1 includes the repression of nuclear movements that are normally associated with the execution of anaphase.
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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.