ArticlePLoS biology2010
CDC5 inhibits the hyperphosphorylation of the checkpoint kinase Rad53, leading to checkpoint adaptation.
Article in PLoS biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- 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
- Dosage suppressors of gpn2ts mutants and functional insights into the role of Gpn2 in budding yeast.PloS one · 2024Article
- Homologous recombination suppresses transgenerational DNA end resection and chromosomal instability in fission yeast.Nucleic acids research · 2023Article
- The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction.Genetics · 2023Article
- Insights into cell robustness against lignocellulosic inhibitors and insoluble solids in bioethanol production processes.Scientific reports · 2022Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- Moonlighting at the Poles: Non-Canonical Functions of Centrosomes.Frontiers in cell and developmental biology · 2022Review
- Adaptation to DNA damage as a bet-hedging mechanism in a fluctuating environment.Royal Society open science · 2021Article
- Cell-cycle phospho-regulation of the kinetochore.Current genetics · 2021Review
- Review
- DNA damage kinase signaling: checkpoint and repair at 30 years.The EMBO journal · 2019Review
- Adaptation in replicative senescence: a risky business.Current genetics · 2019Review
- DNA Damage Stress: Cui Prodest?International journal of molecular sciences · 2019Review
- Adaptation to DNA damage checkpoint in senescent telomerase-negative cells promotes genome instability.Genes & development · 2018Article
- 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
- Inhibition of Polo-like kinase 1 during the DNA damage response is mediated through loss of Aurora A recruitment by Bora.Oncogene · 2017Article
- Reduced kinase activity of polo kinase Cdc5 affects chromosome stability and DNA damage response in S. cerevisiae.Cell cycle (Georgetown, Tex.) · 2016Article
- Multiplexed Imaging of Protein Phosphorylation on Membranes Based on Ti(IV) Functionalized Nanopolymers.Chembiochem : a European journal of chemical biology · 2016Article
- Mitotic entry in the presence of DNA damage is a widespread property of aneuploidy in yeast.Molecular biology of the cell · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The Saccharomyces cerevisiae polo-like kinase Cdc5 promotes adaptation to the DNA damage checkpoint, in addition to its numerous roles in mitotic progression. The process of adaptation occurs when cells are presented with persistent or irreparable DNA damage and escape the cell-cycle arrest imposed by the DNA damage checkpoint. However, the precise mechanism of adaptation remains unknown. We report here that CDC5 is dose-dependent for adaptation and that its overexpression promotes faster adaptation, indicating that high levels of Cdc5 modulate the ability of the checkpoint to inhibit the downstream cell-cycle machinery. To pinpoint the step in the checkpoint pathway at which Cdc5 acts, we overexpressed CDC5 from the GAL1 promoter in damaged cells and examined key steps in checkpoint activation individually. Cdc5 overproduction appeared to have little effect on the early steps leading to Rad53 activation. The checkpoint sensors, Ddc1 (a member of the 9-1-1 complex) and Ddc2 (a member of the Ddc2/Mec1 complex), properly localized to damage sites. Mec1 appeared to be active, since the Rad9 adaptor retained its Mec1 phosphorylation. Moreover, the damage-induced interaction between phosphorylated Rad9 and Rad53 remained intact. In contrast, Rad53 hyperphosphorylation was significantly reduced, consistent with the observation that cell-cycle arrest is lost during adaptation. Thus, we conclude Cdc5 acts to attenuate the DNA damage checkpoint through loss of Rad53 hyperphosphorylation to allow cells to adapt to DNA damage. Polo-like kinase homologs have been shown to inhibit the ability of Claspin to facilitate the activation of downstream checkpoint kinases, suggesting that this function is conserved in vertebrates.
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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.