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The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction

Héloïse Coutelier, Oana Ilioaia, Jeanne Le Peillet, Marion Hamon, Damien D’Amours, View ORCID ProfileMaria Teresa Teixeira, View ORCID ProfileZhou Xu
doi: https://doi.org/10.1101/2021.10.20.465143
Héloïse Coutelier
1Sorbonne Université, PSL, CNRS, UMR8226, Institut de Biologie Physico-Chimique, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, F-75005 Paris, France
2Sorbonne Université, CNRS, UMR7238, Institut de Biologie Paris-Seine, Laboratory of Computational and Quantitative Biology, 75005 Paris, France
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Oana Ilioaia
2Sorbonne Université, CNRS, UMR7238, Institut de Biologie Paris-Seine, Laboratory of Computational and Quantitative Biology, 75005 Paris, France
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Jeanne Le Peillet
2Sorbonne Université, CNRS, UMR7238, Institut de Biologie Paris-Seine, Laboratory of Computational and Quantitative Biology, 75005 Paris, France
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Marion Hamon
1Sorbonne Université, PSL, CNRS, UMR8226, Institut de Biologie Physico-Chimique, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, F-75005 Paris, France
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Damien D’Amours
3Ottawa Institute of Systems Biology, Department of Cellular and Molecular Medicine, University of Ottawa, Roger Guindon Hall, 451 Smyth Road, Ottawa, ON K1H 8M5, Canada
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Maria Teresa Teixeira
1Sorbonne Université, PSL, CNRS, UMR8226, Institut de Biologie Physico-Chimique, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, F-75005 Paris, France
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Zhou Xu
2Sorbonne Université, CNRS, UMR7238, Institut de Biologie Paris-Seine, Laboratory of Computational and Quantitative Biology, 75005 Paris, France
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  • ORCID record for Zhou Xu
  • For correspondence: zhou.xu@polytechnique.org
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Abstract

Telomere dysfunction activates the DNA damage checkpoint to induce a cell cycle arrest. After an extended period of time, however, cells can bypass the arrest and undergo cell division despite the persistence of the initial damage, a process called adaptation to DNA damage. The Polo kinase Cdc5 in Saccharomyces cerevisiae is essential for adaptation and for many other cell-cycle processes. How the regulation of Cdc5 in response to telomere dysfunction relates to adaptation is not clear. Here, we report that Cdc5 protein level decreases after telomere dysfunction in a Mec1-, Rad53- and Ndd1-dependent manner. This regulation of Cdc5 is important to maintain long-term cell cycle arrest but not for the initial checkpoint arrest. We find that both Cdc5 and the adaptation-deficient mutant protein Cdc5-ad are heavily phosphorylated and several phosphorylation sites modulate adaptation efficiency. The PP2A phosphatases are involved in Cdc5-ad phosphorylation status and contribute to adaptation mechanisms. We finally propose that Cdc5 orchestrates multiple cell cycle pathways to promote adaptation.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted October 20, 2021.
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The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction
Héloïse Coutelier, Oana Ilioaia, Jeanne Le Peillet, Marion Hamon, Damien D’Amours, Maria Teresa Teixeira, Zhou Xu
bioRxiv 2021.10.20.465143; doi: https://doi.org/10.1101/2021.10.20.465143
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The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction
Héloïse Coutelier, Oana Ilioaia, Jeanne Le Peillet, Marion Hamon, Damien D’Amours, Maria Teresa Teixeira, Zhou Xu
bioRxiv 2021.10.20.465143; doi: https://doi.org/10.1101/2021.10.20.465143

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