Axon formation as a model of structure-function relationship
Project/Area Number |
24370086
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Developmental biology
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Research Institution | The University of Tokyo |
Principal Investigator |
TABATA TETSUYA 東京大学, 分子細胞生物学研究所, 教授 (10183865)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥18,200,000 (Direct Cost: ¥14,000,000、Indirect Cost: ¥4,200,000)
Fiscal Year 2014: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2012: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
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Keywords | ショウジョウバエ / Sickie / アクチン / Cofilin / slingsohot / Rac / キノコ体 / 軸索伸長 / slingshot / Slingshot |
Outline of Final Research Achievements |
The Drosophila mushroom body (MB) has been well studied as a model of neuronal development and function. We identified two novel genes, sickie and Disco interacting protein 2 (DIP2) that are required for MB development. (1) Sickie regulates F-actin-mediated axonal growth via the non-canonical Rac-Cofilin pathway in a Slingshot (Ssh) -dependent manner. Cofilin plays an essential role as a regulator of axonal growth by severing and depolymerizing F-actin. P-Cofilin levels were increased in the pupal brain of sickie mutants. (2) DIP2 may catalyse the binding of ATP to an as-yet-unidentified substrate with its ATP-synthase domain in theα/βKenyon cells. We propose that DIP2 is regulated by JNK and regulates axon growth and axon branch formation by regulating planar cell polarity in the growth cone. As candidates of its downstream targets, we identified graikit and crumbs genes.
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Report
(4 results)
Research Products
(12 results)
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[Journal Article] The NAV2 homolog Sickie regulates F-actin-mediated axonal growth in Drosophila mushroom body neurons via the non-canonical Rac-Cofilin pathway2014
Author(s)
Abe, T., Yamazaki, D., Murakami, S., Hiroi, M., Nitta, Y., Maeyama, Y., and Tabata T.
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Journal Title
Development
Volume: 141
Issue: 24
Pages: 4716-4728
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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