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An Accumulation of p34cdc2at the End of Mouse Oocyte Growth Correlates with the Acquisition of Meiotic Competence

Growing incompetent mouse oocytes released from follicular cells are unable to spontaneously resume meiosisin vitro.To identify the reasons for meiotic incompetence in these cells, the levels of p34cdc2/cyclin B kinase and p42MAPKbetween incompetent and competent oocytes were compared. p34cdc2was pr...

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Bibliographic Details
Published in:Developmental biology 1996-03, Vol.174 (2), p.335-344
Main Authors: de Vantéry, C., Gavin, A.C., Vassalli, J.D., Schorderet-Slatkine, S.
Format: Article
Language:English
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Summary:Growing incompetent mouse oocytes released from follicular cells are unable to spontaneously resume meiosisin vitro.To identify the reasons for meiotic incompetence in these cells, the levels of p34cdc2/cyclin B kinase and p42MAPKbetween incompetent and competent oocytes were compared. p34cdc2was present at very low levels in incompetent oocytes and accumulated abruptly at the time of meiotic competence acquisition. By contrast, cyclin B and p42MAPKwere present at similar concentrations in both types of oocytes. Okadaic acid induced centrosome phosphorylation and meiotic reinitiation in incompetent oocytes, without inducing an increase in p34cdc2concentration. However, the p34cdc2present in incompetent oocytes was activated and all events following germinal vesicle breakdown were induced up to the formation of a metaphase I spindle including p42MAPKactivation, sustained increase in p34cdc2kinase activity, and translational activation of a dormant mRNA. We suggest that a threshold level of p34cdc2has to be reached for meiotic reinitiation to be spontaneously triggered: competence is restricted at a point preceding MPF activation. Whatever the mechanism involved in this restriction point, i.e., subthreshold concentration of p34cdc2and/or lack of an activator or presence of an inhibitor, it is bypassed by okadaic acid. Downstream of this point meiosis progresses up to metaphase I, even though p34cdc2concentration remains low.
ISSN:0012-1606
1095-564X
DOI:10.1006/dbio.1996.0078