| Project/Area Number |
25891008
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Developmental biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
GOTOH Yukiko 東京大学, 大学院薬学系研究科, 教授 (70252525)
NAKAYAMA I. Keiichi 九州大学, 生体防御医学研究所, 教授 (80291508)
IMAYOSHI Itaru 京都大学ウイルス研究所, 白眉プロジェクト, 特定准教授 (60543296)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 神経幹細胞 / 細胞分裂 / 起源 / p57 / 細胞周期 |
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| Outline of Final Research Achievements |
The mechanism by which adult neural stem cells (NSCs) are established during development is unclear. In this study, analysis of cell-cycle progression by H2B-GFP retention analysis reveals that, in a subset of mouse embryonic neural progenitor cells (NPCs), the cell cycle slows down between E13.5-E15.5 while other embryonic NPCs continue to divide rapidly. By allowing H2B-GFP expressed at E9.5 to become diluted in dividing cells until the young adult stage, we show that a majority of NSCs in the young adult subependymal zone (SEZ) originate from these slowly dividing embryonic NPCs. The cyclin-dependent kinase (CDK) inhibitor p57 is highly expressed in this embryonic subpopulation and the deletion of p57 impairs the emergence of adult NSCs. Our results suggest that a substantial fraction of adult SEZ-NSCs is derived from a slowly dividing subpopulation of embryonic NPCs and identify p57 as a key factor in generating this embryonic origin of adult SEZ-NSCs.
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