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Control of mitotic exit by PP2A regulation of Cdc25C and Cdk1

Craig M Forester1, Jessica Maddox, Justin V Louis

  • 1Department of Oncological Sciences and Center for Children, Huntsman Cancer Institute, Salt Lake City, UT 84112, USA.

Proceedings of the National Academy of Sciences of the United States of America
|December 7, 2007
PubMed

Insights

PP2A:B56delta regulates Cdc25C phosphatase activity, controlling Cdk1 inactivation for mitotic exit. Its failure causes delayed mitosis exit, highlighting its role in cell cycle regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Maturation-promoting factor (MPF) inactivation, involving Cdk1/Cyclin B, is crucial for mitotic exit.
  • While Cyclin B degradation is key, Cdk1 inactivation precedes it, suggesting other regulatory mechanisms are involved.
  • Cdc25C phosphatase activates Cdk1 at the G2/M transition, and PP2A:B56delta deactivates Cdc25C during interphase.

Purpose of the Study:

  • To investigate the role of PP2A:B56delta in regulating Cdc25C activity during mitosis.
  • To determine the impact of PP2A:B56delta dysfunction on Cdk1 activity and mitotic exit.
  • To elucidate the upstream regulatory role of PP2A:B56delta in controlling Cdk1 activity during the cell cycle.

Main Methods:

  • Studied PP2A:B56delta regulation of Cdc25C during mitosis.
  • Utilized stable knockdown and germ-line mouse knockout (KO) of B56delta.
  • Assessed Cdk1 activity, Cdc25C phosphorylation, and Wee1 kinase expression.

Main Results:

  • PP2A:B56delta dephosphorylates Cdc25C at mitosis.
  • Failure of PP2A:B56delta leads to sustained Cdc25C and Cdk1 activation, delaying mitotic exit.
  • B56delta deficiency induces compensatory Wee1 kinase upregulation for cell survival.

Conclusions:

  • PP2A:B56delta is a critical negative regulator of Cdc25C during mitosis.
  • Dysfunctional PP2A:B56delta disrupts Cdk1 inactivation, causing delayed mitotic progression.
  • PP2A:B56delta acts as a key upstream regulator of Cdk1 activity upon exit from mitosis.

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