ArticlePLoS genetics2013
Inhibition of the mitotic exit network in response to damaged telomeres.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 29 citations in OpenAlex.
- Artificial intelligence in mitotic checkpoint modeling: transforming our understanding of cellular division through machine learning and predictive biology.Briefings in bioinformatics · 2026Review
- Yeast centrosomes act as organizing centers to promote Polo kinase-mediated adaptation to persistent DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Characterization of a novel interaction of the Nup159 nucleoporin with asymmetrically localized spindle pole body proteins and its link with autophagy.PLoS biology · 2023Article
- Coupling DNA Replication and Spindle Function inCells · 2021Review
- Rad9-mediated checkpoint activation is responsible for elevated expansions of GAA repeats in CST-deficient yeast.Genetics · 2021Article
- Article
- The regulation of Net1/Cdc14 by the Hog1 MAPK upon osmostress unravels a new mechanism regulating mitosis.Cell cycle (Georgetown, Tex.) · 2020Review
- A guiding torch at the poles: the multiple roles of spindle microtubule-organizing centers during cell division.Cell cycle (Georgetown, Tex.) · 2020Review
- Review
- DNA damage kinase signaling: checkpoint and repair at 30 years.The EMBO journal · 2019Review
- DNA double-strand breaks in telophase lead to coalescence between segregated sister chromatid loci.Nature communications · 2019Article
- Adaptation in replicative senescence: a risky business.Current genetics · 2019Review
- Article
- Functions and regulation of the Polo-like kinase Cdc5 in the absence and presence of DNA damage.Current genetics · 2018Review
- The budding yeast Polo-like kinase localizes to distinct populations at centrosomes during mitosis.Molecular biology of the cell · 2017Article
- Checkpoint adaptation: Keeping Cdc5 in the T-loop.Cell cycle (Georgetown, Tex.) · 2016Article
- Reduced kinase activity of polo kinase Cdc5 affects chromosome stability and DNA damage response in S. cerevisiae.Cell cycle (Georgetown, Tex.) · 2016Article
- Colletotrichum orbiculare Regulates Cell Cycle G1/S Progression via a Two-Component GAP and a GTPase to Establish Plant Infection.The Plant cell · 2015Article
- Asymmetry of the budding yeast Tem1 GTPase at spindle poles is required for spindle positioning but not for mitotic exit.PLoS genetics · 2015Article
- When genome integrity and cell cycle decisions collide: roles of polo kinases in cellular adaptation to DNA damage.Systems and synthetic biology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When chromosomal DNA is damaged, progression through the cell cycle is halted to provide the cells with time to repair the genetic material before it is distributed between the mother and daughter cells. In Saccharomyces cerevisiae, this cell cycle arrest occurs at the G2/M transition. However, it is also necessary to restrain exit from mitosis by maintaining Bfa1-Bub2, the inhibitor of the Mitotic Exit Network (MEN), in an active state. While the role of Bfa1 and Bub2 in the inhibition of mitotic exit when the spindle is not properly aligned and the spindle position checkpoint is activated has been extensively studied, the mechanism by which these proteins prevent MEN function after DNA damage is still unclear. Here, we propose that the inhibition of the MEN is specifically required when telomeres are damaged but it is not necessary to face all types of chromosomal DNA damage, which is in agreement with previous data in mammals suggesting the existence of a putative telomere-specific DNA damage response that inhibits mitotic exit. Furthermore, we demonstrate that the mechanism of MEN inhibition when telomeres are damaged relies on the Rad53-dependent inhibition of Bfa1 phosphorylation by the Polo-like kinase Cdc5, establishing a new key role of this kinase in regulating cell cycle progression.
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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.