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Updated: Feb 24, 2026

Using Mouse Oocytes to Assess Human Gene Function During Meiosis I
Published on: April 10, 2018
Cyclin A2 modulates kinetochore-microtubule attachment in meiosis II
Qing-Hua Zhang1,2, Wai Shan Yuen3,2, Deepak Adhikari3,2
1Development and Stem Cell Program, Monash Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia qing-hua.zhang@monash.edu.
Abstract:
Cyclin A2 is a crucial mitotic Cdk regulatory partner that coordinates entry into mitosis and is then destroyed in prometaphase within minutes of nuclear envelope breakdown. The role of cyclin A2 in female meiosis and its dynamics during the transition from meiosis I (MI) to meiosis II (MII) remain unclear. We found that cyclin A2 decreases in prometaphase I but recovers after the first meiotic division and persists, uniquely for metaphase, in MII-arrested oocytes. Conditional deletion of cyclin A2 from mouse oocytes has no discernible effect on MI but leads to disrupted MII spindles and increased merotelic attachments. On stimulation of exit from MII, there is a dramatic increase in lagging chromosomes and an inhibition of cytokinesis. These defects are associated with an increase in microtubule stability in MII spindles, suggesting that cyclin A2 mediates the fidelity of MII by maintaining microtubule dynamics during the rapid formation of the MII spindle.
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