Wee1B, Myt1, and Cdc25 function in distinct compartments of the mouse oocyte to control meiotic resumption.
Wee1B, Myt1, and Cdc25 function in distinct compartments of the mouse oocyte to control meiotic resumption.
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DOI：
10.1083/jcb.200907161
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发表时间：
2010-01-25
期刊：
影响因子：
--
通讯作者：
Conti M
中科院分区：
文献类型：
--
作者：
Oh JS;Han SJ;Conti M
将Wee 1B保持在细胞核中对于维持减数分裂停滞是重要的，但它的及时输出也是减数分裂恢复所必需的。哺乳动物卵母细胞在第一阶段（GV期）经过长时间的静止后，通过激活Cdc 2-细胞周期蛋白B复合物（促成熟因子[MPF]）重新进入减数分裂。MPF的活性受Wee 1/Myt 1激酶和Cdc 25磷酸酶的调节。在这项研究中，我们表明，隔离的组件，调节MPF活动在不同的亚细胞隔室是必不可少的，他们在减数分裂过程中的功能。Wee 1B或Myt 1的下调导致部分减数分裂恢复，只有当两种蛋白质都下调时，卵母细胞才重新进入细胞周期。在GV分解（GVBD）之前不久，Cdc 25 B从细胞质易位到细胞核，而Wee 1B从细胞核输出到细胞质。这些运动分别由PKA失活和MPF激活调节。错误定位的Wee 1B或Myt 1不能维持减数分裂停滞。因此，Wee 1B，Myt 1和Cdc 25的合作需要维持减数分裂停滞和搬迁这些组件之前GVBD是必要的减数分裂折返。
Keeping Wee1B in the nucleus is important to maintain meiotic arrest, but its timely export is also required for meiosis to resume. After a long period of quiescence at dictyate prophase I, termed the germinal vesicle (GV) stage, mammalian oocytes reenter meiosis by activating the Cdc2–cyclin B complex (maturation-promoting factor [MPF]). The activity of MPF is regulated by Wee1/Myt1 kinases and Cdc25 phosphatases. In this study, we demonstrate that the sequestration of components that regulate MPF activity in distinct subcellular compartments is essential for their function during meiosis. Down-regulation of either Wee1B or Myt1 causes partial meiotic resumption, and oocytes reenter the cell cycle only when both proteins are down-regulated. Shortly before GV breakdown (GVBD), Cdc25B is translocated from the cytoplasm to the nucleus, whereas Wee1B is exported from the nucleus to the cytoplasm. These movements are regulated by PKA inactivation and MPF activation, respectively. Mislocalized Wee1B or Myt1 is not able to maintain meiotic arrest. Thus, cooperation of Wee1B, Myt1, and Cdc25 is required to maintain meiotic arrest and relocation of these components before GVBD is necessary for meiotic reentry.
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影响因子：
5.3
作者：
Longtine, MS;Theesfeld, CL;Lew, DJ
通讯作者：
Lew, DJ
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影响因子：
2.5
作者：
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影响因子：
56.9
作者：
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影响因子：
11.4
作者：
OOKATA, K;HISANAGA, S;KISHIMOTO, T
通讯作者：
KISHIMOTO, T
影响因子：
11.4
作者：
Okamoto, K;Nakajo, N;Sagata, N
通讯作者：
Sagata, N