Progesterone regulates the accumulation and the activation of Eg2 kinase in Xenopus oocytes

M Frank-Vaillant1, O Haccard, C Thibier

  • 1Laboratoire de Physiologie de la Reproduction, INRA/ESA-CNRS 7080, Université Pierre et Marie Curie, boîte 13, 75252 Paris Cédex 05, France.

Insights

Progesterone induces Eg2 protein accumulation in Xenopus oocytes, but this protein kinase is not required for Cdc2 activation during meiotic resumption. Eg2 may organize meiotic spindles.

Area of Science:

  • Cellular and Molecular Biology
  • Developmental Biology
  • Reproductive Biology

Background:

  • Xenopus oocytes resume meiosis upon progesterone stimulation, a process dependent on new protein synthesis and reduced PKA activity.
  • The Aurora/Ipl1 family of protein kinases plays conserved roles in cell division across species.

Purpose of the Study:

  • To investigate the role of Eg2, a Xenopus Aurora/Ipl1 family kinase, in meiotic resumption.
  • To determine if Eg2 accumulation or activity is required for Cdc2 activation in Xenopus oocytes.

Main Methods:

  • Studied Eg2 protein and mRNA levels in response to progesterone and parthenogenetic activation.
  • Utilized an anti-sense strategy to assess the necessity of Eg2 accumulation for Cdc2 activation.
  • Assayed Eg2 kinase activity in relation to Cdc2 activation.

Main Results:

  • Eg2 protein accumulates in response to progesterone, independent of mRNA polyadenylation or cap methylation, and is degraded after parthenogenetic activation.
  • Eg2 accumulation is induced by decreased PKA activity, preceding Cdc2 activation, but Eg2 kinase activity requires Cdc2.
  • Eg2 accumulation is not essential for the signaling pathway leading to Cdc2 activation.

Conclusions:

  • Eg2 protein is not required for progesterone-induced Cdc2 activation in Xenopus oocytes.
  • Eg2 kinase activity is regulated by Cdc2, suggesting a feedback mechanism or downstream role.
  • Eg2 may be involved in meiotic spindle organization, consistent with the known functions of Aurora kinases.