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Cyclin-Dependent Kinases: Their Role in Cell Physiology and Pathologies

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (20 January 2025) | Viewed by 872

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Special Issue Editors

Prof. Dr. Jacek Z. Kubiak

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Guest Editor

Dynamics and Mechanics of Epithelia Group, Faculty of Medicine, Institute of Genetics and Development of Rennes, University of Rennes, CNRS, UMR 6290, 35043 Rennes, France
Interests: embryo development; cell cycle; gene regulation; cancer; stem cells; gonads; genetic diseases
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Prof. Dr. Malgorzata Kloc

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Transplant Immunology, The Houston Methodist Research Institute, Houston, TX 77030, USA
Interests: macrophages; actin cytoskeleton; RhoA pathway; chronic rejection; transplantation; germ cells; stem cells; Xenopus laevis; development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cyclin-dependent kinases include over 13 highly conserved serine-threonine kinases present in eukaryotic cells and play pivotal roles in cell physiology. The founding member of the CDK family—CDK1—is the major cell-cycle regulatory kinase necessary for both S- and M-phases. Monomeric CDKs have very low activity. They are activated by association with their respective cyclins, which play the roles of regulatory subunits of the CDK/cyclin complexes. CDKs activities are also regulated by phosphorylation/dephosphorylation on particular amino acids and by their association with small proteins that act as CDK inhibitors. Besides the cell cycle, CDKs also regulate transcription, mRNA processing, and cell differentiation. Some CDKs are necessary for the activation of other CDKs. Recent studies have shown the important involvement of CDKs in different human diseases, with cancers being the most obvious. They are also extremely important during embryo development. This Special Issue of IJMS includes a broad range of basic and translational articles, both original research reports and reviews, focused on the latest developments in the regulation of cellular process and molecular pathways involving CDKs. This Issue focuses on the role of CDKs, but papers devoted to their regulatory subunits—cyclins and CDK inhibitors—are also welcomed.

Dr. Jacek Z. Kubiak
Prof. Dr. Malgorzata Kloc
Guest Editors

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Keywords

cyclin-dependent kinases
cyclins
CDK inhibitors
cell cycle
cancers
transcription
mRNA processing
differentiation
embryo development

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Research

14 pages, 2385 KiB

Open AccessArticle

CDC6 Inhibits CDK1 Activity in MII-Arrested Oocyte Cell-Free Extract

by Louis Dillac, Klaudia Porębska, Malgorzata Kloc, Rafal P. Piprek, Jean-Pierre Tassan and Jacek Z. Kubiak

Int. J. Mol. Sci. 2025, 26(9), 4309; https://doi.org/10.3390/ijms26094309 - 1 May 2025

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Abstract

The control of cyclin-dependent kinase 1 (CDK1) kinase activity is crucial for cell cycle progression. Cell division cycle 6 (CDC6) inhibits this activity in embryonic mitoses, and thus regulates the timing of cell division progression. The meiotic cell cycle differs greatly from the mitotic one. Metaphase II (MII)-arrested oocytes remain in prolonged M-phase state due to the high activity of CDK1 in the presence of CytoStatic Factor (CSF). The role of CDC6 in the control of CDK1 during MII and oocyte activation remains unknown. Here, we studied the role of CDC6/CDK1 interactions in Xenopus laevis cell-free extracts arrested in MII (CSF extract) and upon calcium activation leading to meiotic-to-mitotic transition. The CSF extract allows analysis of biochemical processes based on immunodepletion of selected proteins and facilitates manipulations using addition of recombinant proteins. We show by glutathione S-transferase (GST)-CDC6 pull-down that CDC6 associates with CDK1 in CSF extract and by histone H1 kinase assay that it downregulates CDK1 activity. Thus, CDC6-dependent inhibition of CDK1 is involved in the homeostasis of the MII-arrest. Upon CSF extract activation with calcium exogenous GST-CDC6 provokes accelerated transition from MII to interphase, while the depletion of endogenous CDC6 results in a slower transition to interphase. We demonstrate this by following both the phosphorylation state of CDK1 substrate cell division cycle 27 (CDC27) and histone H1 kinase assay. Importantly, increasing doses of GST-CDC6 proportionally accelerate CDK1 inactivation showing that CDC6 controls the dynamics of MII to interphase transition in a dose-dependent manner. Thus, CDC6 is a CDK1 silencer acting upon both the MII arrest and CSF extract activation by assuring the physiological activity of CDK1 during this meiotic arrest and correct timely inactivation of this kinase during the second process. Thus, we show that CDC6 controls CDK1 not only during mitotic divisions, but also in MII-arrest and the meiotic-to-mitotic transition in Xenopus laevis cell-free extracts. This study aims to bridge that gap by investigating CDC6 function using a biochemically controlled system. Full article

(This article belongs to the Special Issue Cyclin-Dependent Kinases: Their Role in Cell Physiology and Pathologies)

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