| Project/Area Number |
23791021
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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 |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
HADA Yusuke 東京大学, 医学部附属病院, 助教 (20436463)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 発生・分化 / 遺伝子 / ゲノム / 糖尿病 / 脂肪細胞 / 分化 / エピゲノム / エピジェネティックス / クロマチン / ヒストン / エピジェネティクス |
|---|
| Research Abstract |
In this study, we demonstrate that the PPARγ promoter is marked by both H3K4me3 and H3K27me3 modifications, i.e. the bivalent modification, in ES cells, murine embryonic fibroblasts (MEFs) and adipocyte progenitor cells in white adipose tissue whereas it is marked by only H3K4me3 in mature adipocytes and adipogenic cell lines including 3T3-L1. Upon differentiation, MEFs lose H3K27me3 at the PPARγ promoter and it resolves to H3K4me3 only. Knockdown of the enzymes that regulate the bivalent modification by siRNA blocks adipocyte differentiation. These findings imply that epigenetic regulation of PPARγ expression in in vivo adipocyte progenitor cells plays an important role inadipocyte differentiation.
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