| Project/Area Number |
18500257
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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 |
Neuroscience in general
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| Research Institution | Tokyo Metropolitan Organization for Medical Research |
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Principal Investigator |
OKADO Haruo Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for Neuroscience, staff scientist (60221842)
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| Co-Investigator(Kenkyū-buntansha) |
MIWA Akiko Tokyo Metropolitan Organization for Medical Research, staff scientist (60142155)
MARUYAMA Chiaki Tokyo Metropolitan Organization for Medical Research, staff scientist (00281626)
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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 |
¥4,110,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | RP58 / cerebral cortex / calretini / 転写抑制因子 / Calretinin / アポトーシス / カルビンジン |
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| Research Abstract |
Cerebral Cortex is a brain structure that is developed in the higher orgasm, and function in the memory formation and cognition Recently, we identified a novel transcription factor POZ-zinc finger protein, RP58. We found that this transcript is expressed predominantly in the cerebral cortex in the embryonic stage. In particular, it is expressed faintly in the VZ and strongly in the subventricular zone and cortical plate region. To understand the function of RP58, we generated the RP58-deficient mice. The RP58-null mouse shows the hypoplasia of cerebral cortex and cerebellum. In the cerebral cortex, the formation of subplate layer is markedly retarded. The formation of inside-out pattern also retarded. The double-labeling with IdU and BrdU suggested that the generation of the late-born neurons is delayed. Furthermore, the late-born neurons show abnormal enhancement of calrtinin-immunoreactivity Reporter-assay experiment suggested the RP58 directly supressed the expression of calretinin. These results suggested that RP58 is essential for normal generation of the late-born neurons via the regulation of neurogenin expression.
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