Molecular regulation governing the bilateral palatal shelf adhesion and causing cleft palate in embryonic mice

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592780
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Morphological basic dentistry
• Research Institution: The Nippon Dental University
• Principal Investigator: TAYA YUJI 日本歯科大学, 生命歯学部, 准教授 (30197587)
• Co-Investigator(Kenkyū-buntansha): SOENO Yuuichi 日本歯科大学, 生命歯学部, 講師 (70350139) ; SATO Kaori 日本歯科大学, 生命歯学部, 講師 (90287772) ; AOBA Takaaki 日本歯科大学, 生命歯学部, 教授 (30028807) ; FUJITA Kazuya 日本歯科大学, 生命歯学部, 助教 (70549055)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 歯学 / 病理学 / マウス胎仔 / 二次口蓋発生 / 突起間接着 / 口蓋裂 / 遺伝子発現 / microRNA

Outline of Final Research Achievements

We herein focused on the molecular mechanism governing the cell adhesion of the medial edge epithelia (MEE) of secondary palatal shelves in mouse embryos. To this end, we dissected out of MEE cells of palatal shelves at E14.0-14.5. The expression levels and subcellular localizations of Cask and its related genes/proteins in MEE cells were examined using DNA microarray analysis, LMD/real-time PCR and immunohistochemistry. F11r and Cdkn1a were detected only in MEE cells at the stage of contact, while Cask, Dlg1, Lin7c, Id1 and Tcfe2a were expressed in both MEE and mesenchymal cells. 7 miRNAs regulating the expression of F11r and Cdkn1a were also identified. The nuclear translocation of Cask in MEE cells at the same stage was verified. Our data suggest that Cask and its related molecules contribute to not only the cell adhesion but also cell cycle arrest of MEE at the stage of contact and unique miRNAs may act on their events through the regulation of Cask-related gene expression.

Free Research Field

医歯薬学