2022 Fiscal Year Final Research Report
Dynamic regulation of neural circuit remodeling by scrap & build system
| Project Area | Dynamic regulation of brain function by Scrap & Build system |
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| Project/Area Number |
16H06456
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| Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Emoto Kazuo 東京大学, 大学院理学系研究科(理学部), 教授 (80300953)
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| Co-Investigator(Kenkyū-buntansha) |
小澤 岳昌 東京大学, 大学院理学系研究科(理学部), 教授 (40302806)
今井 猛 九州大学, 医学研究院, 教授 (70509851)
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| Project Period (FY) |
2016-06-30 – 2021-03-31
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| Keywords | 可塑性 / シナプス / 樹状突起 / ショウジョウバエ / 変態 |
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| Outline of Final Research Achievements |
Developing neurons often remove existing compartments such as axons, dendrites, and synapses to refine functionally nascent circuits in a compartment-specific manner, yet how neurons selectively eliminate distinct compartments remains elusive. Drosophila sensory neurons provide an excellent model system to investigate the molecular and cellular mechanisms underlying developmental neuronal remodeling, as larval neurons are extensively remodeled to establish adult-specific circuits during metamorphosis. For the past decade, we have studied the mechanisms of developmental dendrite pruning in Drosophila sensory neurons during metamorphosis. Here we show that presynapses/axons as well as dendrites are eliminated in Drosophila sensory neurons during metamorphosis. To understand the molecular mechanisms of the presynapse/axon elimination, we performed a genetic screen and found that the ubiquitin proteasome systems is required for the presynapse/axon elimination as well as dendrite pruning.
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| Free Research Field |
神経科学
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| Academic Significance and Societal Importance of the Research Achievements |
脳神経回路の可塑性と頑強性は、神経細胞が自らの突起やシナプスの一部を選択的に除去もしくは付加できる能力に起因するが、その制御メカニズムについてはほとんど理解されていない。本研究を推進することにより、神経回路スクラップ＆ビルドを制御する新たな分子細胞基盤と作動原理を明らかにし、研究分野を牽引できる可能性が高い。また、神経回路スクラップ＆ビルド異常が自閉症など発達障害の一因であることが指摘されており、本研究を推進することにより、神経回路スクラップ＆ビルドを担う基本分子メカニズムを明らかにすることは、将来的に発達障害の予防や治療に貢献し得る基礎データやモデルシステムを提供できる可能性がある
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