Analysis of the mechanisms underlying the maintenance/differentiation of neural stem cells and brain development/evolution in mammals
Project/Area Number |
15K06773
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
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Research Institution | Kyoto University |
Principal Investigator |
OHTSUKA Toshiyuki 京都大学, ウイルス・再生医科学研究所, 准教授 (20324709)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Project Status |
Completed (Fiscal Year 2017)
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Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | 神経幹細胞 / 神経発生 / 脳発生 / 脳進化 / HES / 脳形態形成 / Hes |
Outline of Final Research Achievements |
We analyzed the expression and functions of human HES factors that play a central role in the maintenance of neural stem cells (NSCs) and revealed the activities of HES1/4/5 to inhibit neuronal differentiation and maintain NSCs when overexpressed. And we found that both HES1 and HES4 are expressed in the ventricular zone of brains of cynomolgus monkey embryos. The transgenic mice, in which Hes is overexpressed in NSCs of brains by using the Tet-ON system, showed a phenotype of expanded ventricles with thinner cortical plate, due to the maintenance of NSCs and inhibition of neuronal differentiation. In the Hes1-overexpressing Tg mice, basal radial glia-like cells increased in number, suggesting that the alteration in Hes expression levels contributes to the mammalian brain evolution.
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Report
(4 results)
Research Products
(12 results)
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[Journal Article] The Parkinson's Disease-Associated Protein Kinase LRRK2 Modulates Notch Signaling through the Endosomal Pathway.2015
Author(s)
Imai Y, Kobayashi Y, Inoshita T, Meng H, Arano T, Uemura K, Asano T, Yoshimi K, Zhang CL, Matsumoto G, Ohtsuka T, Kageyama R, Kiyonari H, Shioi G, Nukina N, Hattori N, Takahashi R
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Journal Title
PLoS Genet.
Volume: 11
Issue: 9
Pages: e1005503-e1005503
DOI
NAID
Related Report
Peer Reviewed / Open Access
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