SGK phosphorylates Cdc25 and Myt1 to trigger cyclin B-Cdk1 activation at the meiotic G2/M transition

被引:29
|
作者
Hiraoka, Daisaku [1 ]
Hosoda, Enako [2 ]
Chiba, Kazuyoshi [2 ]
Kishimoto, Takeo [1 ]
机构
[1] Ochanomizu Univ, Sci & Educ Ctr, Tokyo, Japan
[2] Ochanomizu Univ, Dept Biol Sci, Tokyo, Japan
来源
JOURNAL OF CELL BIOLOGY | 2019年 / 218卷 / 11期
基金
日本学术振兴会;
关键词
MATURATION-PROMOTING FACTOR; BETA-GAMMA-SUBUNIT; OOCYTE MATURATION; CELL-CYCLE; SIGNALING PATHWAY; PLK1; ACTIVATION; PROTEIN-KINASE; MOTIF PHOSPHORYLATION; XENOPUS OOCYTE; MITOTIC ENTRY;
D O I
10.1083/jcb.201812122
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The kinase cyclin B-Cdk1 complex is a master regulator of M-phase in both mitosis and meiosis. At the G2/M transition, cyclin B-Cdk1 activation is initiated by a trigger that reverses the balance of activities between Cdc25 and Wee1/Myt1 and is further accelerated by autoregulatory loops. In somatic cell mitosis, this trigger was recently proposed to be the cyclin A-Cdk1/Plk1 axis. However, in the oocyte meiotic G2/M transition, in which hormonal stimuli induce cyclin B-Cdk1 activation, cyclin A-Cdk1 is nonessential and hence the trigger remains elusive. Here, we show that SGK directly phosphorylates Cdc25 and Myt1 to trigger cyclin B-Cdk1 activation in starfish oocytes. Upon hormonal stimulation of the meiotic G2/M transition, SGK is activated by cooperation between the G beta gamma-PI3K pathway and an unidentified pathway downstream of G beta gamma, called the atypical G beta gamma pathway. These findings identify the trigger in oocyte meiosis and provide insights into the role and activation of SGK.
引用
收藏
页码:3597 / 3611
页数:15
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