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CNRS-CRBM, 1919 route de Mende, 34293 Montpellier cedex 05, France
* Present address: ICRF/Richard Dimbleby Department of Cancer Research, St Thomas Hospital, Lambeth Palace Road, London SE1 7EH, UK
Author for correspondence (e-mail: mandart{at}crbm.cnrs-mop.fr)
Accepted 8 February 2002
The resumption of meiosis in Xenopus arrested oocytes is triggered by progesterone, which leads to polyadenylation and translation of Mos mRNA, then activation of MAPK pathway. While Mos protein kinase has been reported to be essential for re-entry into meiosis in Xenopus, arrested oocytes can undergo germinal vesicle breakdown (GVBD) independently of MAPK activation, leading us to question what the Mos target might be if Mos is still required. We now demonstrate that Mos is indeed necessary, although is independent of the MAPK cascade, for conversion of inactive pre-MPF into active MPF. We have found that Myt1 is likely to be the Mos target in this process, as Mos interacts with Myt1 in oocyte extracts and Mos triggers Myt1 phosphorylation on some sites in vivo, even in the absence of MAPK activation. We propose that Mos is involved, not only in the MAPK cascade pathway, but also in a mechanism that directly activates MPF in Xenopus oocytes.
Key words: MAPK, Mos, MPF, Myt1, Oocyte maturation, Xenopus
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