2001 Fiscal Year Final Research Report Summary
Molecular Neurogenetic studies on thermosensation ane temperature memory formatio
Project/Area Number |
10440227
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
遺伝
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Research Institution | Nagoya University |
Principal Investigator |
MORI Ikue Nagoya University, Graduate School of Science, Associate Professor, 大学院・理学研究科, 助教授 (90219999)
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Project Period (FY) |
1998 – 2000
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Keywords | Nematode / C. elegans / Behavior / thermotaxis / hearing and memory / Molecular genetics / Neural Network / Sensory signaling |
Research Abstract |
In collaboration with Nef lab, we show that the neuron-specific calcium sensor NCS-1, a highly conserved protein through evolution, is essential for thermotaxis. ncs-1 knockout animals show strong defects in ; isothermoal tracking. The knockout phenotype can be rescued by re-introducing wild-type NCS-1 into the AIY interneuron, a key component of the thermotaxis network. A loss of function form of NCS-1 : unable to bind calcium does not restore thermotaxis, whereas overexpression of NCS-1 enhances isothermal tracking behavior. Thus, proper calcium signaling via the calcium sensor NCS-1 defines a novel pathway that is essential for associative learning and memory in C. elegans. ttx-1 mutants show cryophylic phenotype. In collaboration with Sengupta lab, we show that ttx-1 encodes a member of the highly conserved OTX/OTD homeodomain protein family, and is expressed in the AFD neurons. Misexpression of ttx-1 is sufficient to convert other sensory neurons to AFD-like fate. C. elegans animals bearing a loss-of-function mutation in TAX-6, a calcineurin A subunit, exhibit pleiotropic abnormalities including many aberrant sensory behaviors. The tax-6 mutant defect in thermosensation is consistent with hyperactivation of the AFD thermosensory neurons. Conversely, constitutive activation of TAX-6 causes a behavioral phenotype consistent with inactivation of AFD neurons. In olfactory neurons, the impaired olfactory response of tax-6 mutants to an AWC-sensed odorant is caused by hyper-adaptation, which is suppres'sible by a mutation causing defective olfactory adaptation. Taken together, our results suggest that stimulus-evoked calcium entry activates calcineurin, which in turn negatively regulates multiple aspects of sensory signaling.
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Research Products
(11 results)
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[Publications] Komatsu, H., Jin, Y.-H., L'Etoile, N., <Mori. I.>________-, Bargmann, C.I., Akaike, N. and Ohshima, Y: "Functional reconstitution of alpha and beta subunits of the C. elegans cyclic nucleotide-gated channels."Brain Research. 821. 160-168 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] Gomez, M., De Castro, E., Guarin, E.,Sasakura, H., Kuhara, A., <Mori. I.>________-, Bartfai, T., Bargmann,C.I.and Nef,P.: "Ca^<2+> signaling via the neuronal calcium sensor-1 regulates associate learning and memory in C. elegans"Neuron. 30. 241-248 (2001)
Description
「研究成果報告書概要(欧文)」より
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