Akt inhibits Myt1 the signalling pathway that leads to meiotic G2/M-phase transitions
Akt inhibits Myt1 the signalling pathway that leads to meiotic G2/M-phase transitions
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DOI：
10.1038/ncb741
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发表时间：
2002-02-01
影响因子：
21.3
通讯作者：
Kishimoto, T
中科院分区：
文献类型：
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作者：
Okumura, E;Fukuhara, T;Kishimoto, T
在真核生物中，进入细胞周期的M期是由细胞周期蛋白B-Cdc 2激酶的激活诱导的。在G2期，其灭活剂（Wee 1蛋白激酶家族成员）的活性超过其激活剂Cdc 25 C磷酸酶。然而，在M期进入的情况是相反的，这样的Cdc 25 C的活性超过Wee 1家族。这种逆转的机制尚不清楚。在这里，我们表明，在卵母细胞从海星，激酶Akt（或蛋白激酶B（PKB））磷酸化和下调Myt 1，Wee 1家族的成员。这开关调节活性的平衡，并导致细胞周期蛋白B-Cdc 2在减数分裂G2/M-阶段转换的初始激活。这些发现确定Myt 1作为Akt的新靶点，并证明Akt作为M期启动子发挥作用。
In eukaryotes, entry into M-phase of the cell cycle is induced by activation of cyclin B-Cdc2 kinase. At G2-phase, the activity of its inactivator, a member of the Wee1 family, of protein kinases, exceeds that of its activator, Cdc25C phosphatase. However, at M-phase entry the situation is; reversed, such that the activity of Cdc25C exceeds that of the Wee1 family. The mechanism of this reversal is unclear. Here we show that in oocytes from the starfish Asterina pectinifera, the kinase Akt (or protein kinase B (PKB)) phosphorylates and downregulates Myt1, a member of the Wee1 family. This switches the balance of regulator activities and causes the initial activation of cyclin B-Cdc2 at the meiotic G2/M-phase transition. These findings identify Myt1 as a new target of Akt, and demonstrate that Akt functions as an M-phase initiator.