Inactivation of mitotic kinase triggers translocation of MEN components to mother-daughter neck in yeast
Inactivation of mitotic kinase triggers translocation of MEN components to mother-daughter neck in yeast
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DOI：
10.1091/mbc.e03-04-0238
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发表时间：
2003-11-01
影响因子：
3.3
通讯作者：
Surana, U
中科院分区：
文献类型：
--
作者：
Lim, HH;Yeong, FM;Surana, U
有丝分裂期间，染色体分离、有丝分裂退出和胞质分裂按此顺序执行。尽管已经提出了协调姐妹染色单体分离和有丝分裂退出启动的方案，但将胞质分裂的开始与有丝分裂退出暂时联系起来的机制尚不清楚。有丝分裂的退出受到有丝分裂退出网络 (MEN) 的调节，其中包括 GTPase (Tem1) 和各种激酶（Cdc15、Cdc5、Dbf2 和 Dbf20）。在这里，我们证明 Dbf2 和 Dbf20 功能对于胞质分裂的执行是必需的。这些蛋白质从纺锤体极体重新定位到母体颈部似乎对于这一作用是必要的，因为 cdc15-2 突变细胞虽然能够在半允许温度下退出有丝分裂，但无法将 Dbf2（和 Dbf20）定位到“颈部”并且无法进行胞质分裂。这些细胞可以正常组装和收缩肌动球蛋白环，但无法形成隔膜，这表明 MEN 成分对于隔膜形成的启动至关重要。有趣的是，Dbf2和Dbf20的纺锤体极体到颈部的易位是由有丝分裂激酶的失活触发的。因此，MEN 成分易位至分裂位点所需的激酶失活提供了一种机制，使有丝分裂退出成为胞质分裂的先决条件。
Chromosome segregation, mitotic exit, and cytokinesis are executed in this order during mitosis. Although a scheme coordinating sister chromatid separation and initiation of mitotic exit has been proposed, the mechanism that temporally links the onset of cytokinesis to mitotic exit is not known. Exit from mitosis is regulated by the mitotic exit network (MEN), which includes a GTPase (Tem1) and various kinases (Cdc15, Cdc5, Dbf2, and Dbf20). Here, we show that Dbf2 and Dbf20 functions are necessary for the execution of cytokinesis. Relocalization of these proteins from spindle pole bodies to mother daughter neck seems to be necessary for this role because cdc15-2 mutant cells, though capable of exiting mitosis at semipermissive temperature, are unable to localize Dbf2 (and Dbf20) to the "neck" and fail to undergo cytokinesis. These cells can assemble and constrict the actomyosin ring normally but are incapable of forming a septum, suggesting that MEN components are critical for the initiation of septum formation. Interestingly, the spindle pole body to neck translocation of Dbf2 and Dbf20 is triggered by the inactivation of mitotic kinase. The requirement of kinase inactivation for translocation of MEN components to the division site thus provides a mechanism that renders mitotic exit a prerequisite for cytokinesis.