| First Author | Oh JS | Year | 2011 |
| Journal | Science | Volume | 332 |
| Issue | 6028 | Pages | 462-5 |
| PubMed ID | 21454751 | Mgi Jnum | J:171197 |
| Mgi Id | MGI:4948986 | Doi | 10.1126/science.1199211 |
| Citation | Oh JS, et al. (2011) Protein tyrosine kinase Wee1B is essential for metaphase II exit in mouse oocytes. Science 332(6028):462-5 |
| abstractText | 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. |
