| Project/Area Number |
23792121
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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 |
Functional basic dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
HATA Kenji 大阪大学, 歯学研究科, 准教授 (80444496)
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| Co-Investigator(Renkei-kenkyūsha) |
NISHIMURA Riko 大阪大学, 歯学研究科, 教授 (60294112)
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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: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 軟骨細胞 / Sox9 / 転写因子 |
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| Research Abstract |
Sox9 is a transcription factor critical for endochondral ossification; however, proof of its epigenetic regulation remains elusive. Here, we identified Arid5b (AT-rich interactive domain 5b) as a novel transcriptional co-regulator for Sox9. Arid5b physically interacted with Sox9 and cooperatively promoted chondrogenesis through direct binding to the Col2a1gene promoter. Arid5b^-/-mice showed growth retardation with delayed chondrogenesis. The methylation level of H3K9 in chondrogenic marker gene promoters was markedly increased in Arid5b^-/- chondrocytes. In conclusion, our findings establish a novel epigenomic mechanism of skeletal development, where Arid5b promotes chondrogenesis by facilitating a relationship between Sox9 and Phf2-mediated histone demethylation of chondrogenic gene promoters.
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