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MAP kinase does not inactivate, but rather prevents the cyclin degradation pathway from being turned on in Xenopus

A Abrieu1, T Lorca, J C Labbé

  • 1Centre de Recherches de Biochimie Macromoléculaire, U 240 INSERM, Montpellier, France.

Journal of Cell Science
|January 1, 1996
PubMed

Insights

The c-mos proto-oncogene prevents cyclin degradation in frog eggs by activating MAP kinase. This MAP kinase activation must occur before cyclin B-cdc2 kinase promotes degradation, effectively blocking the pathway.

Area of Science:

  • Cell cycle regulation
  • Meiosis
  • Molecular biology

Background:

  • Unfertilized frog eggs arrest at the second meiotic metaphase.
  • This arrest is mediated by the c-mos proto-oncogene (CSF), which has cytostatic activity.
  • Mitogen-activated protein kinase (MAPK) is hypothesized to mediate CSF's suppression of cyclin degradation.

Purpose of the Study:

  • To confirm the role of MAPK in mediating c-mos proto-oncogene activity.
  • To elucidate the mechanism by which MAPK suppresses cyclin degradation.
  • To investigate the interplay between MAPK, cyclin B-cdc2 kinase, and Ca2+/calmodulin-dependent protein kinase II (CaMKII) in regulating cyclin degradation.

Main Methods:

  • An in vitro assay was developed to generate CSF activity.
  • Recombinant CL 100 phosphatase was used to inactivate MAPK.
  • A constitutively active mutant of CaMKII was employed to study Ca2+ effects.

Main Results:

  • The c-mos proto-oncogene blocks cyclin degradation via MAPK activation.
  • MAPK must be activated before cyclin B-cdc2 kinase effectively promotes cyclin degradation, preventing the degradation pathway from initiating.
  • CaMKII can activate cyclin degradation even in the presence of MPF and c-mos, without inactivating MAPK.

Conclusions:

  • MAPK acts as a preventative factor, not an inactivator, of the cyclin degradation pathway.
  • The timing of MAPK activation is critical for its function in suppressing cyclin degradation.
  • CaMKII-mediated signaling offers an alternative pathway for cyclin degradation independent of MAPK inactivation.

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