細胞間接着装置を介した力と生化学情報の相互制御
キーワード:細胞接着、アクトミオシン骨格、情報伝達、セルコミュニケーション
2017.06.
松沢 健司(まつざわ けんじ) | データ更新日:2023.06.15 |
主な研究テーマ
研究業績
主要原著論文
1. | Kenji Matsuzawa, Hayato Ohga, Kenta Shigetomi, Tomohiro Shiiya, Masanori Hirashima, Junichi Ikenouchi, MAGIs regulate aPKC to enable balanced distribution of intercellular tension for epithelial sheet homeostasis., Communications Biology, 10.1038/s42003-021-01874-z, 4, 1, 337-337, 2021.03, Constriction of the apical plasma membrane is a hallmark of epithelial cells that underlies cell shape changes in tissue morphogenesis and maintenance of tissue integrity in homeostasis. Contractile force is exerted by a cortical actomyosin network that is anchored to the plasma membrane by the apical junctional complexes (AJC). In this study, we present evidence that MAGI proteins, structural components of AJC whose function remained unclear, regulate apical constriction of epithelial cells through the Par polarity proteins. We reveal that MAGIs are required to uniformly distribute Partitioning defective-3 (Par-3) at AJC of cells throughout the epithelial monolayer. MAGIs recruit ankyrin-repeat-, SH3-domain- and proline-rich-region-containing protein 2 (ASPP2) to AJC, which modulates Par-3-aPKC to antagonize ROCK-driven contractility. By coupling the adhesion machinery to the polarity proteins to regulate cellular contractility, we propose that MAGIs play essential and central roles in maintaining steady state intercellular tension throughout the epithelial cell sheet.. |
2. | Kenji Matsuzawa, Takuya Himoto, Yuki Mochizuki, Junichi Ikenouchi, α-Catenin Controls the Anisotropy of Force Distribution at Cell-Cell Junctions during Collective Cell Migration., Cell reports, 10.1016/j.celrep.2018.05.070, 23, 12, 3447-3456, 2018.06, [URL], Adherens junctions (AJs) control epithelial cell behavior, such as collective movement and morphological changes, during development and in disease. However, the molecular mechanism of AJ remodeling remains incompletely understood. Here, we report that the conformational activation of α-catenin is the key event in the dynamic regulation of AJ remodeling. α-catenin activates RhoA to increase actomyosin contractility at cell-cell junctions. This leads to the stabilization of activated α-catenin, in part through the recruitment of the actin-binding proteins, vinculin and afadin. In this way, α-catenin regulates force sensing, as well as force transmission, through a Rho-mediated feedback mechanism. We further show that this is important for stable directional alignment of multiple cells during collective cell movement by both experimental observation and mathematical modeling. Taken together, our findings demonstrate that α-catenin controls the establishment of anisotropic force distribution at cell junctions to enable cooperative movement of the epithelial cell sheet.. |
学会活動
研究資金
科学研究費補助金の採択状況(文部科学省、日本学術振興会)
2022年度~2024年度, 基盤研究(C), 代表, 運動性の細胞集団が秩序を獲得するまでの分子メカニズムの解明.
2019年度~2021年度, 基盤研究(C), 代表, 集団細胞運動における細胞接着の可塑性の制御と役割.
2018年度~2019年度, 若手研究, 代表, 張力シグナルと生化学シグナルの相互制御による集団細胞運動の協調性確立メカニズム.
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九大関連コンテンツ
QIR 九州大学学術情報リポジトリ システム情報科学研究院
理学部・理学研究院
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