| Project/Area Number |
16300120
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
MITANI Shohei Tokyo Women's Medical University, Physiology, Associate Professor, 医学部, 助教授 (90192757)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥12,100,000 (Direct Cost: ¥12,100,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2004: ¥8,500,000 (Direct Cost: ¥8,500,000)
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| Keywords | chemosensation / C.elegans / gene knock out / chemotaxis / body size / C.elegans / G蛋白質共役型受容体 / 信号伝達 / 化学受容体 / 転写因子 |
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| Research Abstract |
It is important to understand how animals feel and distinguish a large number of odorants. The receptors for odorants are transported to the tips of the sensory neurons by intraflagellar transport molecules. Thus, intraflagellar transport (IFT) is essential machinery for biogenesis and maintenance of cilia in many eukaryotic and prokaryotic cells. A large number of polypeptides are known to be involved in IFT, but the physiological role of each component is not fully elucidated. We identified a C.elegans orthologue of a Chlamydomonas reinhardtii IFT component, IFT-81, and found that its loss-of-function mutants show an unusual behavioral property and small body size. The moving area of the mutants is restricted to narrow compared to that of wild-type animals.
IFT-81 is expressed in sensory neurons, and localized at the base of cilia. The similar phenotypes with ift-81 mutants were also observed in several IFT mutants, suggesting these defects are caused by inability of IFT. We also demonstrated that IFT-81 interacts and co-localizes with IFT-74, which is another putative component of IFT. We isolated deletion mutant alleles for the ift-74 gene. The ift-74 loss-of-function mutants showed phenocopies with ift-81 mutants, suggesting IFT-81 and IFT-74 play comparable functions. Moreover, ift-81 and ift-74 mutants similarly exhibited weak anomalies in cilia formation and obvious disruptions of transport in mature cilia. Thus, we conclude that IFT-81 and IFT-74 coordinately act in IFT in C.elegans sensory cilia.
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