2011 Fiscal Year Final Research Report
Molecular mechanism of non-genomic action of ecdysone
| Project/Area Number |
21380035
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied entomology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IWAMI Masafumi 金沢大学, 自然システム学系, 教授 (40193768)
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| Co-Investigator(Renkei-kenkyūsha) |
FUJIMOTO Yoshinori 東京工業大学, 理工学研究科, 教授 (50173472)
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| Project Period (FY) |
2009 – 2011
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| Keywords | エクジソン / カイコガ / 絹糸腺 / 細胞死 / グルコース / オキシダーゼ / 膜受容体 |
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| Research Abstract |
Although it is generally accepted thatecdysoneexerts itseffects through binding with nuclear ecdysone receptor, other receptor on plasma membrane acts as a ecdysone receptor(mEcR) that mediates ecdysone action without gene expression(non-genomic action). mEcR is suggested pharmacologically to be G protein-coupled receptor(GPCR). The activated GPCR activates the signal transduction pathway, which culminates caspase 3-like protease activation and induces cell death. In addition, we showed that ecdysone action against cell death was regulated non-endocrinologically. Anterior silk glands contain glucose oxidase that mediates production of hydrogen peroxide(H_2O_2), and H_2O_2suppresses the ecdysone action, i. e., progression of cell death.
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