Establishment of an animal model for diseases induced by deficiency in cadherin-mediated cell adhesion.

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K14598
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Laboratory animal science
• Research Institution: Kagoshima University
• Principal Investigator: OZAWA Masayuki 鹿児島大学, 医歯学域医学系, 教授 (90136854)
• Co-Investigator(Kenkyū-buntansha): 佐藤 正宏 鹿児島大学, 医用ミニブタ・先端医療開発研究センター, 教授 (30287099)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 細胞接着 / カドヘリン / Cre-loxP系 / トランスジェニックマウス / 病態モデル

Outline of Final Research Achievements

Expression of a chimeric molecule (DECT) composed of a red fluorescent protein (DsRed) and the cytoplasmic domain of E-cadherin (ECT) inhibits the cell surface transport of endogenous cadherins. Thus, establishment of mouse in which DECT expression can be induced time- and space-specific manner provides an animal model for diseases induced by deficiency in cadherin-mediated cell adhesion. We constructed an expression vector that expresses the lacZ reporter gene before Cre-mediated excision and expresses DECT following Cre excision, which removes the lacZ gene. This vector was introduced into ES cells by transfection. The lacZ gene was flanked by loxP sites. The DECT-coding sequence followed the loxP-flanked region. DECT was expected to not be expressed until after Cre excision of β-geo. These clones were found to be positive for β-galactosidase activity and negative for DsRed fluorescence. These ES cells will be used to establish transgenic mouse.

Free Research Field

細胞生物学