Subtype specification of cortical neurons by transcription factors Neurog1/2
| Project/Area Number |
17K07061
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | Keio University |
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Principal Investigator |
Oishi Koji 慶應義塾大学, 医学部(信濃町), 特任講師 (80420818)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 大脳皮質 / 神経系前駆細胞 / 神経分化 / 転写因子 / 脳・神経 / 発生・分化 / 層形成 / Neurogenin |
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| Outline of Final Research Achievements |
The cerebral cortex is composed of hundreds of different subtypes of neurons, which are sequentially generated from common neural progenitor cells. This sequential specification has been interpreted as a result from the sequential changes of differentiation potential of progenitor cells. However, the molecular mechanisms regulating this sequential changes have been poorly understood. We focused on transcription factors Neurog1/2, which are expressed by neural progenitor cells throughout cortical neurogenesis but only participate in subtype specification of deep layer neurons. We found the importance of the temporal regulation of transcriptional activity of Neurog1/2 and the epigenetic regulation by polycomb repressive complexes.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、Neurog1/2による特異的サブタイプ決定メカニズムの分子機構を明らかにし、さらにそれが時期選択的に活性化される機構を明らかにした。すなわち、Neurog1/2によるCTニューロンの分化決定は特定の時期だけで“ON”になるが、この“ON”の状態は、Neurog1/2の転写活性の制御、及びポリコーム抑制複合体によって制御されることが分かった。これまで神経前駆細胞の分化能の時間的変化に関しては、時期依存的な転写因子の発現という単純なモデルが考えられていた。本研究の結果から、「時間的変化」が転写レベルとエピジェネティックなレベルという多階層で制御されることが示唆された。
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Report
(4 results)
Research Products
(16 results)
