Conversions of M-phase onset system from meiosis to early embryonic mitosis

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The Cdc2-cyclin B kinase is a master regulator of M phase. It is kept inactive through its inhibitory phosphorylation by Weel/Myt1 kinases during G2 phase, and activated by Cdc25 phosphatase at the onset of M phase. The presence of these opposing enzyme activities in G2-phase cells indicates that the regulation of their activities is crucial for the G2/M-phase transition. Even though there are many studies about them using many kinds of materials, upper regulatory mechanisms are diverse and unclear. There are possibilities that the difference comes from difference of species and/or difference of developing stages. So I tried to show that the regulation of M-phase onset are changed dependent of the developing stages using unique animal for studying materials. I investigated upstream regulators especially for Myt1 comparing meiosis I, meiosis II and embryonic mitotic cycles through starfish development. In this study, I mainly demonstrated that (i) Ser75site of Myt1 is also phosphoryated at the onset of meiosis II. Akt phosphorylates this site at the onset of meiosis I but the activity of Akt is absent during meiosis II. A candidate of the kinase is p90Rsk which is active during meiosis II and could phosphorylate Myt1 in vitro. Myt1 is also thought to be regulated by Plk1 which is transiently binds with Myt1 at G2/M-phase.(ii) In embryonic mitotic cell, Ser75 of Myt1 is also phosphorylated but Akt and p90Rsk are inactive. A novel kinase is thought to phosphorylate Ser75 of Myt1. I have also tried to identify this kinase, but I could not achieve in this period of aid. Identification of the kinase will be further project for study of the mechanisms of M-phase onset in embryonic mitotic cell cycle.