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Kenji Matsuzawa Last modified date：2023.06.15

Lecturer / Informational Biology
Department of Biology
Faculty of Sciences


Graduate School
Department of Biology
Graduate School of Sciences
Undergraduate School
Department of Biology
School of Sciences
Other Organization
Other
Administration Post
Other


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Homepage
https://kyushu-u.pure.elsevier.com/en/persons/kenji-matsuzawa
　Reseacher Profiling Tool　Kyushu University Pure
Phone
092-802-4294
Academic Degree
PhD
Country of degree conferring institution (Overseas)
No
Field of Specialization
Cell biology
ORCID(Open Researcher and Contributor ID)
0000-0002-9664-0736
Total Priod of education and research career in the foreign country
00years00months
Research
Research Interests
  • Mutual regulation between force and biochemical signaling at cell-cell adhesion in epithelial cells
    keyword : cell-cell adhesion, actomyosin cytoskeleton, signal transduction, cell communication
    2017.06.
Academic Activities
Papers
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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, 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..
Presentations
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Membership in Academic Society
  • The Molecular Biology Society of Japan
  • Japan Society for Cell Biology


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