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Distinct regulators for Plk1 activation in starfish meiotic and early embryonic cycles

Takayuki Okano-Uchida1, Eiichi Okumura, Motoko Iwashita

  • 1Laboratory of Cell and Developmental Biology, Graduate School of Bioscience, Tokyo Institute of Technology, Nagatsuta, Midoriku, Yokohama 226-8501, Japan.

The EMBO Journal
|October 9, 2003
PubMed

Insights

Polo-like kinase 1 (Plk1) is not the trigger for meiotic reinitiation. Instead, Plk1 primarily suppresses Myt1 to activate cyclin B-Cdc2 during cell division.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Polo-like kinase (Plk) regulates mitosis, with Plk1 proposed as a trigger kinase for cyclin B-Cdc2 activation.
  • The upstream regulation of Plk1 activation is not fully understood.

Purpose of the Study:

  • Investigate the upstream regulators of Plk1 activation.
  • Clarify the role of Plk1 in cyclin B-Cdc2 activation during meiotic and embryonic cell cycles.

Main Methods:

  • Studied starfish meiotic and early embryonic cell cycles.
  • Analyzed the interplay between Plk1 and Cdc2 kinases.

Main Results:

  • Identified distinct upstream regulators for Plk1 activation: cyclin B-Cdc2 (meiosis I), MAPK (meiosis II), and cyclin A-Cdc2 (embryonic M-phase).
  • Demonstrated that Plk1 is not the trigger kinase for meiotic reinitiation.
  • Showed Plk1 primarily suppresses Myt1, rather than activating Cdc25, to promote cyclin B-Cdc2 activation.

Conclusions:

  • Plk1 activation is regulated by different kinases at distinct cell cycle stages.
  • Plk1's main role in activating cyclin B-Cdc2 involves Myt1 inhibition.
  • Plk1 can be activated by cyclin A-Cdc2 or cyclin B-Cdc2.

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