| Project/Area Number |
24770186
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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 |
Cell biology
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| Research Institution | Osaka University |
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Principal Investigator |
FUMOTO Katsumi 大阪大学, 医学(系)研究科(研究院), 助教 (40467783)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 上皮細胞 / 頂底極性 / 細胞増殖 / 組織構築 / wnt / 肺 / 分岐形態形成 / 上皮単独培養 / 期間培養 / Wntシグナル / 上皮組織 / 接着 |
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| Research Abstract |
In this study, we aim to elucidate the mechanism for lung branching morphogenesis which is mediated by Wnt signaling. We have already generated three dimensional culture system of lung epithelium. By using this, we treated the epithelium with CHIR99021, an agonist for beta-catenin pathway or transduced lentiviruses that express Wnt2, a typical ligand for beta-catenin dependent pathway. CHIR or Wnt2 promoted branching morphogenesis. Activation of beta-catenin pathway promoted apical constriction provably through enhanced localization of atypical PKCzeta (aPKCzeta), a critical regulator of apical and basal polarity, to apical membrane. In addition, aPKCzeta inhibitor showed the defect in branching morphogenesis and apical constriction. In conclusion, we found that beta-catenin pathway maintains distal progenitor and is required for branching morphogenesis provably through apical targeting of aPKCzeta and apical constriction.
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