| Project/Area Number |
18K17262
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 57070:Developmental dentistry-related
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2018: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 歯 / 細胞間接着因子 / エナメル芽細胞 / 細胞間接着 / 上皮細胞 / 細胞接着 / 分化 / 細胞・組織 / 発生・分化 / シグナル伝達 |
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| Outline of Final Research Achievements |
In previous study, we identified a desmosomal protein PKP1 localized at the tight junction in dental epithelial cells. In this study, we analyzed the mechanism of PKP1 in cell-cell junctions in dental epithelial cells. To investigate the mechanisms of PKP1, we constructed PKP1 knock out cells (KO) by CRISPR/Cas9 system. PKP1 KO cells showed that the localization of ZO-1 to plasma membrane was disturbed. Transfected PKP1-EmGFP rescued ZO-1 distribution in plasma membrane. These data suggest that PKP1 localizes at tight junction and forms complex with ZO-1. PKP1 may play an important role for cell-cell adhesion regulating ZO-1 localization in plasma membrane.
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| Academic Significance and Societal Importance of the Research Achievements |
歯科医学の最終目的は、歯を含む口腔諸器官の再生メカニズムの解明とその臨床応用である。本研究により、外胚葉異形成症原因遺伝子の一つであるPKP1が細胞膜において密着結合構成因子ZO-1の局在制御を通してエナメル芽細胞分化制御を担っている可能性を発見した。これにより新たなエナメル芽細胞分化制御機構の解明の進展が期待される。こうした歯の分化メカニズムを厳密に制御していくことが歯の再生やエナメル質の形成を可能にすると考えられる。
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