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Dephosphorylation of cyclin-dependent kinases by type 2C protein phosphatases

A Cheng1, K E Ross, P Kaldis

  • 1Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, Connecticut 06520-8024, USA.

Genes & Development
|December 2, 1999
PubMed

Insights

Type 2C protein phosphatases (PP2Cs) dephosphorylate cyclin-dependent protein kinases (CDKs), regulating cell cycle progression. This phosphatase activity is conserved across yeast and human cells, impacting CDK regulation.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Cyclin-dependent protein kinases (CDKs) require activating phosphorylation for cell cycle progression.
  • Cdk-activating kinase (CAK) performs this phosphorylation, but the responsible phosphatase remains largely unknown.

Purpose of the Study:

  • To identify the protein phosphatase responsible for dephosphorylating budding yeast CDKs.
  • To investigate the role of PP2Cs in CDK regulation and conservation in human cells.

Main Methods:

  • In vitro and in vivo assays to measure Cdc28p phosphatase activity.
  • Genetic analysis using yeast strains with altered PTC2 and PTC3 gene expression.
  • Analysis of human cell extracts for CDK phosphatase activity.

Main Results:

  • Two yeast PP2Cs, Ptc2p and Ptc3p, were identified as the primary enzymes dephosphorylating Cdc28p.
  • These phosphatases account for approximately 90% of Cdc28p phosphatase activity.
  • PP2C-like enzymes also dephosphorylate human Cdk2, indicating conserved substrate specificity.

Conclusions:

  • Type 2C protein phosphatases (PP2Cs) are the key phosphatases for budding yeast CDK Cdc28p.
  • PP2C regulation of CDKs is evolutionarily conserved from yeast to humans.

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