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PMID:21454751
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| Citation |
Oh, JS, Susor, A and Conti, M (2011) Protein tyrosine kinase Wee1B is essential for metaphase II exit in mouse oocytes. Science 332:462-5 |
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| Abstract |
Waves of cyclin synthesis and degradation regulate the activity of Cdc2 protein kinase during the cell cycle. Cdc2 inactivation by Wee1B-mediated phosphorylation is necessary for arrest of the oocyte at G2-prophase, but it is unclear whether this regulation functions later during the metaphase-to-anaphase transition. We show that reactivation of a Wee1B pathway triggers the decrease in Cdc2 activity during egg activation. When Wee1B is down-regulated, oocytes fail to form a pronucleus in response to Ca(2+) signals. Calcium-calmodulin-dependent kinase II (CaMKII) activates Wee1B, and CaMKII-driven exit from metaphase II is inhibited by Wee1B down-regulation, demonstrating that exit from metaphase requires not only a proteolytic degradation of cyclin B but also the inhibitory phosphorylation of Cdc2 by Wee1B. |
| Links |
PubMed Online version:10.1126/science.1199211 |
| Keywords |
Animals; CDC2 Protein Kinase/antagonists & inhibitors; CDC2 Protein Kinase/metabolism; Calcium/metabolism; Calcium Signaling; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism; Cell Cycle Proteins/genetics; Cell Cycle Proteins/metabolism; Cyclin B/genetics; Cyclin B/metabolism; Down-Regulation; Female; Gene Knockdown Techniques; Maturation-Promoting Factor/metabolism; Meiosis; Metaphase; Mice; Mice, Inbred C57BL; Oocytes/physiology; Phosphorylation; Protein-Tyrosine Kinases/genetics; Protein-Tyrosine Kinases/metabolism; RNA, Messenger/genetics; RNA, Messenger/metabolism |
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