| Co-Investigator(Kenkyū-buntansha) |
KOGA Makoto Kyushu University, Faculty of Science, Assistant Professor, 大学院・理学研究院, 助教授 (60243888)
FUJIWARA Manbi Kyushu University, Faculty of Science, Research Associate, 大学院・理学研究院, 助手 (70359933)
HIROTSU Takaaki Kyushu University, Faculty of Science, Research Associate, 大学院・理学研究院, 助手 (70404035)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Research Abstract |
Animals sense many environmental stimuli, and process the sensory information in the nervous system. This sensory processing includes selection of appropriate information, proper integration, and modification by experience or memory. To elucidate molecular and neuronal mechanisms for such sensory processing, we are conducting genetic studies on behavior and body size, both of which are under the sensory control in C.elegans.
In C.elegans, a secretory protein, HEN-1, and a receptor tyrosine kinase, SCD-2, regulate sensory integration of two sensory signals : aversive copper ion and an attractive odorant diacetyl. In addition, they are required for an associative learning after conditioned with NaCl and starvation. By expressing wild type scd-2 cDNA in scd-2 mutants driven by specific promoters, we found that SCD-2 functions in a few pairs of interneurons at the adult stage. In this year, we investigated molecules that function in these interneurons to regulate sensory processing. Glutamate receptors are candidates of those molecules, because, in C.elegans, three types of glutamate receptors, metabotropic receptors, cationic receptors and anionic receptors, are known to function in the central nervous system. Among those, we found that an AMPA type cationic receptor, GLR-1, regulates the sensory integration in a distinct pathway from HEN-1/SCD-2. In addition, we found that a Cl- channel type glutamate receptor, which has significant homology with GABA_A receptors, also regulates the sensory integration.
In C.elegans, body size is regulated by a TGFb homologue, DBL-1, and downstream transcriptional regulator SMAD, SMA-2 and SMA-4. We screened mutant with defects in this pathway by monitoring an expression level of LON-1, which is regulated by SMA-2 and SMA-4, and identified a new regulatory component, qj1. We revealed that qj1 is a novel protein expressed in hypodermis, and negatively regulates SMA-2 and SMA-4 to control body size of C.elegans.
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