2016 Fiscal Year Final Research Report

A research of chemical biology on regulatory mechanisms of recovery from diapause in C. elegans

Research Project

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Project/Area Number	26292061
Research Category	Grant-in-Aid for Scientific Research (B)
Allocation Type	Partial Multi-year Fund
Section	一般
Research Field	Bioorganic chemistry
Research Institution	Tottori University
Principal Investigator	Kawano Tsuyoshi 鳥取大学, 農学部, 教授 (50270567)
Co-Investigator(Kenkyū-buntansha)	尾添嘉久島根大学, 生物資源科学部, 教授 (80112118)
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)
Project Period (FY)	2014-04-01 – 2017-03-31
Keywords	休眠 / 線虫 / 受容体 / 情報伝達 / ペプチド
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.
Free Research Field	生物有機化学・分子生物学
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。