| Project/Area Number |
25840085
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Developmental biology
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| Research Institution | Tokyo Institute of Technology |
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Principal Investigator |
Enomoto Takayuki 東京工業大学, バイオ研究基盤支援総合センター, 東工大特別研究員 (70635680)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 細胞分化 / 転写因子 / 嗅覚 / 遺伝子発現制御 / 細胞運命決定 / マウス遺伝学 / 感覚神経 / 神経接続 / エピジェネティクス / 細胞運命決定制御 / 嗅覚システム / 神経軸索投射 / 細胞核内構造 / 発言制御 / 嗅覚神経 / 軸索投射 / 嗅覚受容体 / 発現制御 |
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| Outline of Final Research Achievements |
Olfactory sensory neurons (OSNs) detect a vast number of odorous chemicals from the external environment. Each OSN has distinct characteristics by choosing only one from the repertoire of odorant receptor (OR) genes. However, the molecular mechanism underlying the characterization of OSNs is not well understood. In this study, we show that a zinc finger transcription factor Bcl11b is a key regulator for the cell-fate determination of OSNs. In the mouse, OR genes are classified into two groups, classⅠ and classⅡ. During the development of OSNs, an individual OSN is fated to express a single OR gene from either classⅠ or classⅡ OR repertoires. We found that Bcl11b is predominantly expressed in classⅡ OSNs. Loss of Bcl11b function resulted in a severe reduction of classⅡ OSNs, instead in an increase and expansion of classⅠ OSNs. Gain of Bcl11b function mutation decreased classⅠ OSN population and increased classⅡ. Thus, Bcl11b controls the alternative OSN-fates.
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