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Akt inhibits Myt1 in the signalling pathway that leads to meiotic G2/M-phase transition

Eiichi Okumura1, Takeshi Fukuhara, Hitoshi Yoshida

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

Nature Cell Biology
|January 22, 2002
PubMed

Insights

The protein kinase Akt phosphorylates and downregulates Myt1, a Wee1 family kinase. This action initiates M-phase entry by activating cyclin B-Cdc2 kinase during the G2/M transition.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • M-phase entry in eukaryotes is regulated by cyclin B-Cdc2 kinase.
  • Wee1 family kinases inactivate cyclin B-Cdc2, while Cdc25C phosphatase activates it.
  • The mechanism reversing Wee1 and Cdc25C activity at M-phase entry is unknown.

Purpose of the Study:

  • To elucidate the mechanism regulating the switch in Wee1 and Cdc25C activity at the G2/M transition.
  • To identify novel regulators of M-phase initiation.

Main Methods:

  • Studied starfish (Asterina pectinifera) oocytes.
  • Investigated the role of Akt kinase in regulating Myt1, a Wee1 family member.
  • Analyzed the phosphorylation and activity of Myt1 and cyclin B-Cdc2.

Main Results:

  • Akt (protein kinase B) phosphorylates and downregulates Myt1 in starfish oocytes.
  • This action shifts the balance of regulator activities, favoring Cdc25C over Wee1 family kinases.
  • The findings demonstrate Akt's role in initiating cyclin B-Cdc2 activation at the meiotic G2/M transition.

Conclusions:

  • Myt1 is a novel substrate for Akt.
  • Akt functions as a key initiator of M-phase entry by downregulating Wee1 family kinases.
  • This study reveals a new regulatory pathway controlling cell cycle progression.

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