ArticleCell cycle (Georgetown, Tex.)2016
Reduced kinase activity of polo kinase Cdc5 affects chromosome stability and DNA damage response in S. cerevisiae.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 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
- The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction.Genetics · 2023Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- Cell-cycle phospho-regulation of the kinetochore.Current genetics · 2021Review
- The regulation of Net1/Cdc14 by the Hog1 MAPK upon osmostress unravels a new mechanism regulating mitosis.Cell cycle (Georgetown, Tex.) · 2020Review
- Polo kinase recruitment via the constitutive centromere-associated network at the kinetochore elevates centromeric RNA.PLoS genetics · 2020Article
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- A guiding torch at the poles: the multiple roles of spindle microtubule-organizing centers during cell division.Cell cycle (Georgetown, Tex.) · 2020Review
- Cuminal InhibitsMicroorganisms · 2020Article
- Review
- Adaptation in replicative senescence: a risky business.Current genetics · 2019Review
- 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
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo-like kinases (PLKs) control several aspects of eukaryotic cell division and DNA damage response. Remarkably, PLKs are overexpressed in several types of cancer, being therefore a marker of bad prognosis. As such, specific PLK kinase activity inhibitors are already used in clinical trials and the regulation of PLK activation is a relevant topic of cancer research. Phosphorylation of threonine residues in the T-loop of the kinase domain is pivotal for PLKs activation. Here, we show that T238A substitution in the T-loop reduces the kinase activity of Cdc5, the only PLK in Saccharomyces cerevisiae, with minor effect on cell growth in unperturbed conditions. However, the cdc5-T238A cells have increased rate of chromosome loss and gross chromosomal rearrangements, indicating altered genome stability. Moreover, the T238A mutation affects timely localization of Cdc5 to the spindle pole bodies and blocks cell cycle restart after one irreparable double-strand break. In cells responding to alkylating agent metylmethane sulfonate (MMS), the cdc5-T238A mutation reduces the phosphorylation of Mus81-Mms4 resolvase and exacerbates the MMS sensitivity of sgs1Δ cells that accumulate Holliday junctions. Of importance, the previously described checkpoint adaptation defective allele, cdc5-ad does not show reduced kinase activity, defective Mms4 phosphorylation and genetic interaction with sgs1Δ. Our data define the importance of regulating Cdc5 activity through T-loop phosphorylation to preserve genome integrity and respond to DNA damage.
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