SGK regulates pH increase and cyclin B–Cdk1 activation to resume meiosis in starfish ovarian oocytes
Author(s) -
Enako Hosoda,
Daisaku Hiraoka,
Noritaka Hirohashi,
Saki Omi,
Takeo Kishimoto,
Kazuyoshi Chiba
Publication year - 2019
Publication title -
the journal of cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.414
H-Index - 380
eISSN - 1540-8140
pISSN - 0021-9525
DOI - 10.1083/jcb.201812133
Subject(s) - germinal vesicle , biology , cyclin dependent kinase 1 , microbiology and biotechnology , cyclin b , cyclin , meiosis , oogenesis , cyclin b1 , oocyte , cell cycle , cell , biochemistry , embryo , gene
Tight regulation of intracellular pH (pH i ) is essential for biological processes. Fully grown oocytes, having a large nucleus called the germinal vesicle, arrest at meiotic prophase I. Upon hormonal stimulus, oocytes resume meiosis to become fertilizable. At this time, the pH i increases via Na + /H + exchanger activity, although the regulation and function of this change remain obscure. Here, we show that in starfish oocytes, serum- and glucocorticoid-regulated kinase (SGK) is activated via PI3K/TORC2/PDK1 signaling after hormonal stimulus and that SGK is required for this pH i increase and cyclin B-Cdk1 activation. When we clamped the pH i at 6.7, corresponding to the pH i of unstimulated ovarian oocytes, hormonal stimulation induced cyclin B-Cdk1 activation; thereafter, oocytes failed in actin-dependent chromosome transport and spindle assembly after germinal vesicle breakdown. Thus, this SGK-dependent pH i increase is likely a prerequisite for these events in ovarian oocytes. We propose a model that SGK drives meiotic resumption via concomitant regulation of the pH i and cell cycle machinery.
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