| Project/Area Number |
18591866
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Osaka University |
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Principal Investigator |
MURATA Junko Osaka University, Graduate School of Medicine, Assistant Professor (80332740)
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| Co-Investigator(Kenkyū-buntansha) |
KUBO Takeshi Osaka University Graduate School of Medicine, 医学系研究科, Professor (30107031)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,670,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Development of inner ear / Notch signaling pathway / Hair cell / Supporting cell / Cell differentiation / Prosensory region / Notch-Hes1経路 / 蝸牛 / p27Kip1 / Math1 / BrdU陽性細胞 / Notch伝達系 / 感覚上皮前駆細胞 / Hes1 / p27^<Kip1> / 増殖維持 |
|---|
| Research Abstract |
The Notch signaling pathway has been thought to play a crucial role in the development of mammalian inner ear. Supported by the Grant-in-Aid for Scientific Research <KAKENHI> #18591866, we investigated the spatio-temporal activation pattern of Notchl using the antibody that specifically recognizes the activated form of Notchl (actN1) to clarify the multiple roles of the Notch pathway during the inner ear development. Between embryonic days (E) 12.5 and E14.5, actN1 was weakly detected mainly in the medial region of the cochlear epithelium, where Jagged1 (Jag1)-immunoreactivity (IR) was also observed. Jag1-IR gradually became stronger in a more sharply defined area, finally becoming localized in supporting cells, while actN1 was detected in an overlapping area Thus, a positive feed-back loop was assumed to exit between the expression of Jag1 and actN1. In addition, actN1 started to be strongly expressed in the cells surrounding Mathl-positive hair cell progenitors between E14.5 and E15.5. Strong actN1-IR continued in both a supporting cell linege and in the greater epithelial ridge during the perinatal stage but ended by P7, suggesting that Notchl activation may initially demarcate a prosensory region in the cochlear epithelium and then inhibit progenitor cells from becoming hair cells via classical "lateral inhibition."
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