| Project/Area Number |
14360033
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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 |
蚕糸・昆虫利用学
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| Research Institution | KANAZAWA UNIVERSITY |
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Principal Investigator |
SAKURAI Sho KANAZAWA UNIVERSITY, NATURAL SCIENCE AND TECHNOLOGY, PROFESSOR, 自然科学研究科, 教授 (80143874)
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| Co-Investigator(Kenkyū-buntansha) |
IWAMI Masafumi KANAZAWA UNIVERSITY, NATURAL SCIENCE AND TECHNOLOGY, ASSOC.PROFESSOR, 自然科学研究科, 助教授 (40193768)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2004: ¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 2003: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2002: ¥5,600,000 (Direct Cost: ¥5,600,000)
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| Keywords | ecdysteroid / silkworm / anterior silk gland / programmed cell death / steroid hormone / membrane receptor / non-genomic action / 絹糸腺 / 絹系腺 / 細胞死 / アポトーシス / ステロイド |
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| Research Abstract |
Programmed cell death (PCD) of anterior silk glands of the silkworm, Bombyx mori, is induced by 20E elicits its effects via binding with a heterodimeric nuclear receptor (EcR/USP) and acting as a transcriptional factor. In the PCD, however, we found various events associated with the cell death, which cannot be interpreted from the point of view of 20E action via nuclear receptor, and therefore we assumed the presence of a non-genomic action of 20E via ecdysone membrane receptor (mEcR). We confirmed the presence of the binding sites of ecdysteroids on membrane proteins. The responsible protein is embedded in plasma membrane and possesses a high binding activity with ecdysteroids. In addition, we found that 20E increases an intracellular cAMP level as rapidly as 30 seconds after 20E challenge. We also demonstrated that activation of protein kinase C and caspase 3 is involved in the 20E-induced PCD. The PCD precedes via plasma membrane blebbing, cellular shrinkage, DNA oligonucleosomal fragmentation, nuclear condensation, nuclear fragmentation and apoptotic body formation. Blebbing, cell shrinkage and apoptotic body formation are under the control of genomic action of 20E while other events are under the non-genomic action of 20E, probably through mEcR. The present results suggest that a single steroid hormone exerts its physiological effects through both genomic and nongenomic pathways.
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