2007 Fiscal Year Final Research Report Summary
Domain mapping of glial origin … Cell biological basis of glial diversity
| Project/Area Number |
16200028
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | National Institute for Physiological Sciences |
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Principal Investigator |
IKENAKA Kazuhiro National Institute for Physiological Sciences, Molecular Physiology, Professor (00144527)
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| Co-Investigator(Kenkyū-buntansha) |
ONO Katsuhiko National Institute for Physiological Sciences, Molecular Physiology, Associate Professor (30152523)
SEIJI Hitoshi National Institute for Physiological Sciences, Molecular Physiology, Associate Professor (70300895)
TAKEBAYASHI Hirohide National Institute for Physiological Sciences, Molecular Physiology, Assistant Professor (60353439)
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| Project Period (FY) |
2004 – 2007
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| Keywords | Olig2 / astrocyte / oligodendrocyte / Cre / loxP / tamoxifen / forebrain / GLAST / PDGFa receptor |
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| Research Abstract |
We analyzed fates of Olig2 progenitor cells in the forebrain using tamoxifen inducible Cre/loxP system. Tamoxifen was injected to the E 13.5 dams to induce Cre-mediated recombination to label Olig2+ cells and animals were analyzed at E16.5. Approximately 60% of GFP+/Olig2+ cells were positive for GLAST, a marker for astrocyte progenitor cells, in the cortex, and 40% of these cells were positive for PDGFα receptor, a marker for oligodendrocyte progenitor cells. In addition, 9% of GFP+/Olig2+ cell population were immunopositive for class DI β tubulin, a marker for immature neurons. The above value suggests the presence of cells co-expressing both progenitor markers, which is supported by the observation that approximately 15% of GLAST+ cells co-expressed PDGFRα and vice versa in the late fetal stage. Therefore, Olig2+ cells in the late fetal stages were mixed population of glial progenitor cells : The number of astrocyte progenitor cells, which expressed GLAST or FGF receptor 3, decreased in the Olig2 deficient mouse cortex, while that in the knockout basal forebrain was unchanged. Oligodendrocyte progenitor cells were missing almost completely in the Olig2 deficient forebrain, as previously reported. These results indicate that Olig2 is essential for oligodendrocyte genesis and also that it plays some roles in astrocytogenesis in a region-specific manner.
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