Possible role of p38 MAPK-MNK1-EMI2 cascade in metaphase-II arrest of mouse oocytes

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Yu Miyagaki1, Yoshinori Kanemori1, Fumi Tanaka1

  • 1Faculty of Life and Environmental Sciences, University of Tsukuba, Tsukuba Science City, Ibaraki, Japan.

Biology of Reproduction
|June 13, 2014
PubMed

Insights

The Mos-MAPK pathway regulates oocyte arrest. This study reveals a Mos-mediated p38 pathway, alongside the known Mos-MEK1/2 pathway, contributes to metaphase-II arrest in mouse oocytes.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Reproductive Biology

Background:

  • The Mos-MAPK signaling pathway is crucial for metaphase-II arrest in vertebrate oocytes.
  • This pathway involves key components like Mos, MEK1/2, ERK1/2, and EMI2.

Purpose of the Study:

  • To investigate the role of p38, a MAPK subfamily member, in Mos-regulated metaphase-II arrest.
  • To determine if p38 contributes to the metaphase-II arrest mechanism in mouse oocytes.

Main Methods:

  • Mos depletion using morpholino oligonucleotides.
  • Inhibition of p38 and MEK1/2 kinases using chemical inhibitors.
  • Analysis of p38 and EMI2 phosphorylation levels.
  • Assessment of cyclin B1 degradation.

Main Results:

  • Mos depletion significantly reduced p38 phosphorylation.
  • Simultaneous inhibition of p38 and MEK1/2 induced metaphase-II release and cyclin B1 degradation.
  • Inhibition of both kinases abolished EMI2 phosphorylation.
  • MNK1, downstream of p38, was shown to phosphorylate EMI2.

Conclusions:

  • The Mos-mediated p38 pathway is implicated in maintaining metaphase-II arrest.
  • This pathway acts in parallel to the established Mos-MEK1/2 pathway.
  • Both pathways converge to regulate EMI2 phosphorylation and ensure oocyte arrest.
Keywords:
EMI2ERK1/2 MAPKMosmeiosisoocytep38 MAPK

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