| Project/Area Number |
23659035
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biological pharmacy
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| Research Institution | Kyoto University |
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Principal Investigator |
ITOH Nobuyuki 京都大学, 大学院・薬学研究科, 教授 (10110610)
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| Co-Investigator(Renkei-kenkyūsha) |
MIYAKE Ayumi 京都大学, 大学院・薬学研究科, 講師 (40346044)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 分子物学 / 分泌性因子 / 形態形成 / 遺伝子 / ゼブラフィッシュ / マウス |
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| Research Abstract |
We identified a gene encoding a novel secreted protein in mice, humans, and zebrafish including Brorin, Brorin-like, Neucrin, and Fgf22. The inhibition of Brorin and Brorin-like functions in zebrafish resulted in the impairment of neural development. Brorin-like potentially plays roles in neural development and functions. The knockdown of neucrin also suppressed neuronal differentiation and caused increased cell proliferation and apoptosis in developing neural tissues. Neucrin plays roles in neural development in zebrafish. The Fgf22 morphants were defective in proper formation of the MHB constriction and the midbrain. The knockdown of Fgf22 caused decreased cell proliferation in the midbrain, expanded expression of roof plate and tegmental marker genes, and decreased expression of tectal marker genes. Furthermore, Fgf22 partially rescued the Fgf3/fgf8 double morphant phenotype. Fgf22 is involved in midbrain development downstream of Fgf3 and Fgf8 in the MHB but not of Hh in the floor plate.
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