Analysis of novel functions of an atonal homolog in aversive behavior and gap junction formation
| Project/Area Number |
25830018
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
Hori Sayaka 東京女子医科大学, 医学部, 助教 (20470122)
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| Research Collaborator |
MITANI Shohei
IINO Yuichi
ODA Shigekazu
SUEHIRO Yuji
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | synaptogenesis / gap junction / Optogenetics / C. elegans / Aversive behavior / atonal / 光遺伝学 / ギャップ結合 / シナプス選択 / 逃避 / イネキシン / 感覚鈍麻 / 神経発生 / 神経行動学 |
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| Outline of Final Research Achievements |
Animals alter their behavior in response to stimulus strength. Meanwhile, detailed analysis of neural circuit is complicated circuits. So to clarify the neural mechanism of the behavioral switch for danger, we choose C. elegans as a model system, because of advantage for analysis in molecular, circuit, and behavior level. We had screened for genes required for such behavior using optogenetics and RNAi screening, and showed that a transcription factor lin-32, Drosophila atonal homolog, is required for U-turn. Especially, the lin-32 mutants fail to express a gap junction channel inx-1, showing electrical synapse defects. Our finding will clarify the atonal regulation of gap junction formation.
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Report
(4 results)
Research Products
(6 results)
