A mechanism of mechanotransduction at the cell‐cell interface: Emergence of α‐catenin as the center of a force‐balancing mechanism for morphogenesis in multicellular organisms

Abstract

Cells can sense and respond to their mechanical environment, resulting in not only the function of sensory organs for touch, sound or balance, but also proper morphogenesis and differentiation during embryogenesis [1–3]. The conversion of mechanical forces into biochemical signals is called mechanotransduction. Defects in mechanotransduction lead to diseases such as sensory organ disorders, muscular dystrophy, atherosclerosis, osteoporosis, and polycystic kidney disease [4, 5], and mechanotransduction is now an emerging field in biology and medicine. Mechanotransduction has been examined in a variety of cells or organs, such as sensory cells, heart, blood vessels, kidney, bone, and tumors, and in the cell-extracellular matrix adhesion structure (focal adhesion), in which the extracellular matrix and fluid are considered the mechanical environment [6, 7]. In the morphogenesis of multicellular organisms, cells are also important mechanical environment elements because each cell is surrounded by adjacent cells. One type of cell-cell junction structure, the desmosome, plays an important role in resisting mechanical stresses, and may also work as a possible mediator of mechanical signals. Contractile forces generated by a cell provide mechanical stimuli both to itself and to neighboring cells through the adherens junction (AJ), a cell-cell junction structure responsible for intercellular transmission of forces [8–12]. Here, I describe a mechanism of mechanotransduction at AJs based on a-catenin functions, and discuss its significance and molecular mechanisms. Mechanotransduction in general