The molecular mechanism that regulates axonal transport of synaptic vesicle precursors
| Project/Area Number |
17H05010
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Morphology/Structure
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| Research Institution | Tohoku University |
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Principal Investigator |
NIWA SHINSUKE 東北大学, 学際科学フロンティア研究所, 准教授 (30714985)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥26,260,000 (Direct Cost: ¥20,200,000、Indirect Cost: ¥6,060,000)
Fiscal Year 2019: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2018: ¥8,320,000 (Direct Cost: ¥6,400,000、Indirect Cost: ¥1,920,000)
Fiscal Year 2017: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
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| Keywords | 軸索輸送 / KIF1A / シナプス小胞 / ARL8A / ARL8B / BORC / UNC-104 / ARL-8 / 線虫 / arl-8 / JIP3 / unc-16 / キネシン / 神経科学 |
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| Outline of Final Research Achievements |
Neurons transmit information via synaptic vesicles that are localized in the axon. Synaptic vesicles are synthesized only in the cell body and transported down to the axon by a transport mechanism called axonal transport. In this work, we have shown that axonal transport is regulated by a molecular cascade consisting of BLOC-1 related complex (BORC), small GTPase ARL-8 and a molecular motor KIF1A. BORC activates ARL-8 by converting ARL-8(GDP) to ARL-8(GTP). ARL-8(GTP) binds to KIF1A and unlock the autoinhibition. Activated KIF1A binds to axonal transport carriers and transport them.
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| Academic Significance and Societal Importance of the Research Achievements |
軸索輸送は神経細胞の機能を支える重要なマシナリーであるにもかかわらず、その制御についてはほとんどわかっていなかった。また、制御機構があるとしてそれが破綻した場合に何が起こるのかも不明であった。本研究では軸索輸送の制御メカニズムの一端を解明することができた。また、このメカニズムに異常が起こることが遺伝性痙性対麻痺と呼ばれる運動神経疾患の原因となることを明らかにした。
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Report
(4 results)
Research Products
(23 results)
