| Project/Area Number |
26292061
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Bioorganic chemistry
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| Research Institution | Tottori University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
尾添 嘉久 島根大学, 生物資源科学部, 教授 (80112118)
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| Co-Investigator(Renkei-kenkyūsha) |
ICHIYANAGI Tsuyoshi 鳥取大学, 農学部, 教授 (00302240)
YABUTA Yukinori 鳥取大学, 農学部, 准教授 (00379562)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥12,350,000 (Direct Cost: ¥9,500,000、Indirect Cost: ¥2,850,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2015: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2014: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
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| Keywords | 休眠 / 線虫 / 受容体 / 情報伝達 / ペプチド / 生理活性物質 / シグナル伝達 / 生体分子 / 生理活性 |
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| Outline of Final Research Achievements |
In this research, we have identified the receptor for uracil, which induces recovery from larval diapause of the nematode Caenorhabditis elegans, and elucidated the cellular signal transduction. We have also analyzed the regulatory mechanism of larval diapause.
The chemosensory neurons ASJs play an important role in regulation of recovery from larval diapause. We identified a G protein-coupled receptor, SRH-11, which is expressed especially in the ASJs, as a receptor for uracil. It is possible that SRH-11 bound by uracil increases a second messenger, cGMP, concentration to induce the recovery. Moreover, we have demonstrated that short peptides NLP-3 and FLP-21, which are expressed in ASJs, regulate secretion of a TGF-β like protein, DAF-7, and an insulin-like peptide, INS-35, respectively. This secretory regulation possibly modulates larval diapause.
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| Academic Significance and Societal Importance of the Research Achievements |
ネコブセンチュウの農業被害は甚大であり、土壌燻蒸等の環境負荷が大きい防除法は敬遠され、今後、排除されると予想される。そこで、ネコブセンチュウの新たな防除法の開発がも求められている。
本研究はモデル生物・線虫C. elegansの休眠打破（ネコブセンチュウでは宿主浸入後の感染成立）に着目し、その機構を化学生物学的に解明することにより、ネコブセンチュウ防除法の開発に資する。本研究では休眠打破物資がその受容体を介してどのように機能するかを明確した。休眠は多くの種が保有する生存戦略の一つであり、本研究の学術的意義も大きいと考えている。
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