Akt inhibits Myt1 the signalling pathway that leads to meiotic G2/M-phase transitions
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Okumura, E
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Tokyo Inst Technol, Grad Sch Biosci, Lab Cell & Dev Biol, Midori Ku, Yokohama, Kanagawa 2268501, JapanTokyo Inst Technol, Grad Sch Biosci, Lab Cell & Dev Biol, Midori Ku, Yokohama, Kanagawa 2268501, Japan
Okumura, E
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Fukuhara, T
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Yoshida, H
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Hanada, S
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Kozutsumi, R
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Tokyo Inst Technol, Grad Sch Biosci, Lab Cell & Dev Biol, Midori Ku, Yokohama, Kanagawa 2268501, JapanTokyo Inst Technol, Grad Sch Biosci, Lab Cell & Dev Biol, Midori Ku, Yokohama, Kanagawa 2268501, Japan
Kozutsumi, R
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Mori, M
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Tokyo Inst Technol, Grad Sch Biosci, Lab Cell & Dev Biol, Midori Ku, Yokohama, Kanagawa 2268501, JapanTokyo Inst Technol, Grad Sch Biosci, Lab Cell & Dev Biol, Midori Ku, Yokohama, Kanagawa 2268501, Japan
Mori, M
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Tachibana, K
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Kishimoto, T
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[1] Tokyo Inst Technol, Grad Sch Biosci, Lab Cell & Dev Biol, Midori Ku, Yokohama, Kanagawa 2268501, Japan
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.