Regulation of spontaneous meiosis resumption in mouse oocytes by various conventional PKC isozymes depends on cellular compartmentalization

In this study, we investigated the spatio-temporal distribution of conventional protein kinases C (cPKC) isoforms PKC-alpha, PKC-betaI, PKC-betaII and PKC-gamma in mouse oocytes. The cPKCs were present in the cytoplasm at the start of the process and migrated to the nucleus (or germinal vesicle) bef...

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Veröffentlicht in:Journal of cell science 2004-10, Vol.117 (Pt 21), p.4969-4978
Hauptverfasser: Avazeri, Nathalie, Courtot, Anne-Marie, Lefevre, Brigitte
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Sprache:eng
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Zusammenfassung:In this study, we investigated the spatio-temporal distribution of conventional protein kinases C (cPKC) isoforms PKC-alpha, PKC-betaI, PKC-betaII and PKC-gamma in mouse oocytes. The cPKCs were present in the cytoplasm at the start of the process and migrated to the nucleus (or germinal vesicle) before germinal vesicle breakdown, except for PKC-gamma which remained cytoplasmic. In both compartments, the fully phosphorylated form corresponding to the 'mature' enzyme was revealed for PKC-alpha, PKC-betaI and PKC-betaII. Microinjection of specific antibodies against each isozyme in one or the other cell compartment at different times of the meiotic process, permitted us to observe the following: (1) When located in the cytoplasm at the beginning of the process, PKC-alpha is not implicated in germinal vesicle breakdown, PKC-betaI and PKC-gamma are involved in maintaining the meiotic arrest, and PKC-betaII plays a role in meiosis reinitiation. Furthermore, just before germinal vesicle breakdown, these cytoplasmic cPKCs were no longer implicated. (2) When located in the germinal vesicle, PKC-alpha, PKC-betaI and PKC-betaII are involved in meiosis reinitiation. Our data highlight not only the importance of the nuclear pathways in the cell cycle progression, but also their independence of the cytoplasmic ones. Further investigations are however necessary to discover the molecular targets of these cPKCs to better understand the links with the cell cycle progression.
ISSN:0021-9533
1477-9137
DOI:10.1242/jcs.01375