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J Cell Sci. 2013 Mar 1;126(Pt 5):1081-5. doi: 10.1242/jcs.115592. Epub 2013 Jan 23.

Cdc25A activity is required for the metaphase II arrest in mouse oocytes.

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Center for Reproductive Sciences and The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, Department of Obstetrics, Gynecology and Reproductive Sciences at the University of California, San Francisco, CA 94143-0556, USA.


Mammalian oocytes are arrested in metaphase of second meiosis (MII) until fertilization. This arrest is enforced by the cytostatic factor (CSF), which maintains the M-phase promoting factor (MPF) in a highly active state. Although the continuous synthesis and degradation of cyclin B to maintain the CSF-mediated MII arrest is well established, it is unknown whether cyclin-dependent kinase 1 (Cdk1) phosphorylations are involved in this arrest in mouse oocytes. Here, we show that a dynamic equilibrium of Cdk1 phosphorylation is required to maintain MII arrest. When the Cdc25A phosphatase is downregulated, mouse oocytes are released from MII arrest and MPF becomes inactivated. This inactivation occurs in the absence of cyclin B degradation and is dependent on Wee1B-mediated phosphorylation of Cdk1. Thus, our data demonstrate that Cdk1 activity is maintained during MII arrest not only by cyclin turnover but also by steady state phosphorylation.

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