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MAPK pathway activation delays G2/M progression by destabilizing Cdc25B

Puji Astuti1, Tanya Pike, Charlotte Widberg

  • 1Diamantina Institute for Cancer Immunology and Metabolic Medicine, University of Queensland, Brisbane 4102, Queensland, Australia.

The Journal of Biological Chemistry
|October 6, 2009
PubMed

Insights

Mitogen-activated protein kinase (MAPK) pathway activation delays cell cycle G2 phase entry and blocks G2 checkpoint exit. This occurs via MEK1-dependent destabilization of cdc25B, a key G2/M regulator.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • The role of the mitogen-activated protein kinase (MAPK) pathway in G2/M phase progression is debated.
  • Growth factors and phorbol esters activate MAPK signaling, impacting cell cycle progression.

Purpose of the Study:

  • To elucidate the specific role of the MAPK pathway in G2/M phase progression.
  • To investigate the mechanism by which MAPK activation influences entry into mitosis and G2 checkpoint control.

Main Methods:

  • Activation of the MAPK pathway using epidermal growth factor (EGF) or 12-O-tetradecanoylphorbol-13-acetate (TPA).
  • Assessment of G2 phase delay and G2 checkpoint arrest.
  • Investigation of the involvement of MAPK/extracellular signal-regulated kinase kinase 1 (MEK1).
  • Analysis of cdc25B stability and function.

Main Results:

  • MAPK pathway activation induced a G2 phase delay independent of known checkpoint pathways but dependent on MEK1.
  • MAPK signaling blocked exit from G2 checkpoint arrest.
  • MEK1-dependent destabilization of cdc25B mediated the G2 delay and blocked checkpoint exit.
  • Reintroduction of cdc25B rescued the MEK1-dependent G2 delay.

Conclusions:

  • MEK1 has a novel function in controlling G2/M progression by regulating cdc25B stability.
  • MAPK signaling influences mitotic entry timing and G2 checkpoint exit via cdc25B destabilization.
  • This study reveals a new mechanism for MAPK pathway involvement in cell cycle control.

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