title: Two distinct mechanisms control the accumulation of cyclin B1 and Mos in Xenopus oocytes in response to progesterone.
abstract: Progesterone-induced meiotic maturation of Xenopus oocytes requires the synthesis of new proteins, such as Mos and cyclin B. Synthesis of Mos is thought to be necessary and sufficient for meiotic maturation; however, it has recently been proposed that newly synthesized proteins binding to p34(cdc2) could be involved in a signaling pathway that triggers the activation of maturation-promoting factor. We focused our attention on cyclin B proteins because they are synthesized in response to progesterone, they bind to p34(cdc2), and their microinjection into resting oocytes induces meiotic maturation. We investigated cyclin B accumulation in response to progesterone in the absence of maturation-promoting factor-induced feedback. We report here that the cdk inhibitor p21(cip1), when microinjected into immature Xenopus oocytes, blocks germinal vesicle breakdown induced by progesterone, by maturation-promoting factor transfer, or by injection of okadaic acid. After microinjection of p21(cip1), progesterone fails to induce the activation of MAPK or p34(cdc2), and Mos does not accumulate. In contrast, the level of cyclin B1 increases normally in a manner dependent on down-regulation of cAMP-dependent protein kinase but independent of cap-ribose methylation of mRNA.
authors.affiliation: Laboratoire de Physiologie de la Reproduction, Centre National de la Recherche Scientifique, Université Pierre et Marie Curie, Paris 05, France.
authors.forename: M
authors.initials: M
authors.lastname: Frank-Vaillant
authors.forename: C
authors.initials: C
authors.lastname: Jessus
authors.forename: R
authors.initials: R
authors.lastname: Ozon
authors.forename: J L
authors.initials: JL
authors.lastname: Maller
authors.forename: O
authors.initials: O
authors.lastname: Haccard
mesh_terms: D000818:Animals; D016203:CDC2 Protein Kinase / Q000378:metabolism; D019926:Cyclin B / Q000378:metabolism*; D056744:Cyclin B1; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D020930:MAP Kinase Kinase Kinases / Q000378:metabolism*; D016200:Maturation-Promoting Factor / Q000378:metabolism; D008845:Microinjections; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D008938:Mitosis; D019319:Okadaic Acid / Q000494:pharmacology; D009865:Oocytes / Q000187:drug effects / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology*; D011485:Protein Binding; D011494:Protein Kinases / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism; D015398:Signal Transduction; D014981:Xenopus
chemical_list: D019926:Cyclin B; D056744:Cyclin B1; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D011994:Recombinant Proteins; D019319:Okadaic Acid; D011374:Progesterone; D011494:Protein Kinases; C102333:histone H1 kinase; D016203:CDC2 Protein Kinase; D016200:Maturation-Promoting Factor; D020928:Mitogen-Activated Protein Kinases; D020930:MAP Kinase Kinase Kinases