2021 Fiscal Year Final Research Report
The mechanism of ameloblast differentiation associated with apicobasal polarity induced by topological conversion.
Project/Area Number |
20K18786
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 57070:Developmental dentistry-related
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Research Institution | Kyushu University |
Principal Investigator |
Miyazaki Kanako 九州大学, 歯学研究院, 特別研究員(RPD) (30778840)
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Project Period (FY) |
2020-04-01 – 2022-03-31
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Keywords | 歯 / 細胞間接着因子 / 細胞増殖 |
Outline of Final Research Achievements |
Regeneration of teeth is still difficult because of their complex shape. However, clarifying the mechanism of organ-specific morphological changes would be able to bring us closer to tooth regeneration. Previous studies showed that suppression of the desmosomal protein Plakophilin 1 (PKP1) induces smaller tooth size in ex vivo culture method, and PKP1 localizes into the nucleus during the early tooth development stage. However, it remains unclear about the function in the nucleus. In this study, we showed that PKP1 translocates to the nucleus via its own N-terminal nuclear localization sequence. We also identified that PKP1 regulates c-Myc transcription via TCF/LEF, which regulating cell proliferation and tooth size.
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Free Research Field |
歯科矯正学
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Academic Significance and Societal Importance of the Research Achievements |
歯を含む口腔の器官再生は歯科医学の最終目的と言えるが、歯はその形状の複雑さから発生メカニズムの解明やその再生が未だ困難である。本研究によって外胚葉異形成症の原因遺伝子の1つであるPkp1が歯原性上皮細胞の分化の初期段階において核内で転写共役因子として細胞増殖に関与し、歯のサイズに関与している可能性を発見した。この成果は、歯の発生における歯原性上皮幹細胞の新たな機能解明の進展が期待される。歯の分化メカニズムの厳密な制御が可能となれば、将来的に歯の再生やエナメル質形成を可能にすると考えられる。
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