Protein Tyrosine Kinase Wee1B Is Essential for Metaphase II Exit in Mouse Oocytes
作者： J. S. Oh , A. Susor , M. Conti
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摘要: Waves of cyclin synthesis and degradation regulate the activity Cdc2 protein kinase during cell cycle. inactivation by Wee1B-mediated phosphorylation is necessary for arrest oocyte at G2-prophase, but it unclear whether this regulation functions later metaphase-to-anaphase transition. We show that reactivation a Wee1B pathway triggers decrease in egg activation. When down-regulated, oocytes fail to form pronucleus response Ca(2+) signals. Calcium-calmodulin-dependent II (CaMKII) activates Wee1B, CaMKII-driven exit from metaphase inhibited down-regulation, demonstrating requires not only proteolytic B also inhibitory Wee1B.
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