Cyclin A2 modulates kinetochore-microtubule attachment in meiosis II.
Cyclin A2 modulates kinetochore-microtubule attachment in meiosis II.
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DOI:
10.1083/jcb.201607111
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发表时间:
2017-10-02
期刊:
影响因子:
--
通讯作者:
Carroll J
中科院分区:
文献类型:
--
作者:
Zhang QH;Yuen WS;Adhikari D;Flegg JA;FitzHarris G;Conti M;Sicinski P;Nabti I;Marangos P;Carroll J
The role of the Cdk regulatory protein cyclin A2 and its dynamics in female meiosis are unclear. Zhang et al. show that, unlike in mitosis, cyclin A2 persists during metaphase of meiosis II (MII). Cyclin A2 regulates microtubule stability, allows normal MII spindle formation, and prevents merotelic attachments and lagging chromosomes at MII exit. 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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