Mechanisms of membrane regulation of cell-cell adhesion by I-BAR proteins

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K06625
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 44010:Cell biology-related
• Research Institution: Nara Institute of Science and Technology
• Principal Investigator: Nishimura Tamako 奈良先端科学技術大学院大学, 先端科学技術研究科, 助教 (40415261)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: I-BARタンパク質 / 細胞間接着

Outline of Final Research Achievements

The role of cell membranes in cell-cell adhesion formation between epithelial cells is largely unknown. We investigated the role of the I-BAR proteins, which regulate the formation of protruding membranes, in intercellular adhesion formation. The I-BAR proteins were distributed not only in the protruding membrane structures of epithelial cells but also in the cell-cell adhesion. Knocking-out the I-BAR proteins resulted in decreased linearity in tight junctions and decreased actin filaments. Furthermore, knockout of the I-BAR proteins resulted in the impairment of epithelial barrier function. Therefore, it was suggested that the I-BAR proteins may have an important role in the formation and maintenance of the cell-cell adhesion.

Free Research Field

細胞生物学

Academic Significance and Societal Importance of the Research Achievements

本研究により、これまで不明であった細胞間接着の形成における細胞膜の形態制御の重要性が明らかとなった。細胞間接着は、生物の形態形成時に重要であり、I-BARタンパク質のノックアウトマウスは胎生致死を示すとの報告があることから、形態形成における細胞間接着の制御にI-BARタンパク質が関与する可能性が示唆された。また、細胞間接着の形成不全は、がんの浸潤・転移と関連していることから、I-BARタンパク質の機能不全ががんの悪性化に関与する可能性が示唆された。