Molecular analyses of crossing-proof mechanism of dendrites
| Project/Area Number |
24500410
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Kyoto University |
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Principal Investigator |
USUI Tadao 京都大学, 生命科学研究科, 助教 (10324708)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 樹状突起 / 突起間交差忌避 / 細胞間認識タンパク質 / てんかん / 突起間忌避 / 生得行動 / 神経生理 / 神経発生 / カルシウムシグナル / FRET型プローブ |
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| Outline of Final Research Achievements |
Our research group has clarified the essential signaling mechanism of the normal extension of dendrites in the Drosophila model system. We have showed that both seven-transmembrane cadherin molecules Flamingo and intracellular binding molecule Espinas prevented cooperatively the dendrites from crossing with each other. By using RNA interference method and Cas9/CRISPR method, we found that intracellular scaffold protein Neurochondrin, one of the identified group of molecules as Espinas binding factor, displayed a similar crossing defects as that of Espinas mutant.
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Report
(4 results)
Research Products
(8 results)
