遺伝子と栄養の相互作用における樹状突起形成のメカニズム解明

• Project/Area Number: 13F03798
• Research Category: Grant-in-Aid for JSPS Fellows
• Allocation Type: Single-year Grants
• Section: 外国
• Research Field: 森林科学
• Research Institution: Institute of Physical and Chemical Research
• Principal Investigator: MOORE Adrian 国立研究開発法人理化学研究所, 脳科学総合研究センター, チームリーダー (30442932)
• Co-Investigator(Kenkyū-buntansha): MACCHI MARC 国立研究開発法人理化学研究所, 脳科学総合研究センター, 外国人特別研究員 ; MACCHI Marc 独立行政法人理化学研究所, その他部局等, 外国人特別研究員 ; マッキ マーク 独立行政法人理化学研究所, 脳科学総合研究センター, 外国人特別研究員
• Project Period (FY): 2013-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥2,300,000 (Direct Cost: ¥2,300,000); Fiscal Year 2015: ¥600,000 (Direct Cost: ¥600,000); Fiscal Year 2014: ¥1,100,000 (Direct Cost: ¥1,100,000); Fiscal Year 2013: ¥600,000 (Direct Cost: ¥600,000)
• Keywords: dendrite branching / nutrition / Dystrophin / actin cytoskeleton / bactcria / environment / sensory neurons

Outline of Annual Research Achievements

The dendrite arbor is patterned by growing in 2 dimensions (2D) cross the inner surface of the body wall epithelium and in 3D by detaching from the basal lamina of the body wall and invading into the epidermal cell layer. We’ve found that changing nutritional state by raising Drosophila larvae on food containing different amino-acid levels leads to dendritic shape changes and in particular modulating dendrite invasion into underlying epithelial cells. We discovered that Dystrophin promotes the 3D invasions of the epithelial cells by dendrites in a nutrition-dependent manner. In parallel, we monitored endogenous Dystrophin expression and found that Dystrophin was expressed in both sensory neurons and the underlying epidermal cells of the body wall.In summary, our data suggest that a genetic locus disrupted in Autism Spectrum Disorders controls dendrite patterning in response to nutritional state.

Research Progress Status

27年度が最終年度であるため、記入しない。

Strategy for Future Research Activity

27年度が最終年度であるため、記入しない。