| Project/Area Number |
18570076
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Animal physiology/Animal behavior
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| Research Institution | National Institute of Agrobiological Sciences |
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Principal Investigator |
MASAMI Shimoda National Institute of Agrobiological Sciences, Division of insect sciences, Chief researcher (80344000)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,080,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | circadian rhythm / Drosophila melanogaster / biological rhythm / sleep / clock gene / Fragile X syndrome / FMR1 / 行動遺伝子 |
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| Research Abstract |
1. Drosophila FMR1 mutants are models of human fragile X syndrome. They show a loss of locomotor activity rhythm and severe degradation of eclosion timing. We analyzed the circadian behavior of FMR1 mutants in two genetic backgrounds, yellow white (yw) and Canton S (CS). The arrhythmic phenotype of circadian locomotor activity in constant darkness (DD) did not significantly change in either genetic background. Surprisingly, eclosion timing was completely restored by backcrossing the mutant with yw or CS flies. Morphological analysis of the small ventrally located lateral neurons of FMR1 mutants revealed that the dorsal-projection area was significantly larger in arrhythmic than rhythmic flies. In addition, mutants in both genetic backgrounds had a significantly lower evening peak in the light-dark (LD) cycle. These results indicate that lack of FMR1 does not affect eclosion timing, but alters locomotor activity patterns in both LD and DD conditions by affecting the arborization of small ventrally located lateral neurons. Thus, the FMR1 gene may regulate the circadian-related locomotor activity of Drosophila.
2. Genetic and biochemical studies have shown that Drosophila double-time (dbt) and its mammalian ortholog Casein kinase I epsilon (hckl ε) regulate the circadian phosphorylation of period (per). We investigated whether the expression of mammalian casein kinase I can replace the activity of dbt in flies. Global expression of the dbt rescued lethality of the null mutant and rescued flies showed normal locomotor activity rhythms. In constrast, hckI ε did not rescue lethality or locomotor activity of dbt mutants. Furthermore dbt overexpression had only a small effect on period length, whereas hckI ε expression in clock cells greatly lengthened period and increased the arrhythmic flies. These results indicate that hckl ε cannot replace the activity of dbt in flies despite the high degree of similarity in primary sequence and kinase function.
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