Within tissues, key cellular adaptations occur via mechanotransduction responses at cell-cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked to the force-propagating and -generating actomyosin cytoskeleton. Recent studies have found that AJs maintain monolayer integrity in dynamic tissues and drive collective cell behavior by converting into asymmetric remodeling entities. Here, we overview the molecular processes that may explain how asymmetric cell-cell junctions sense differences in cytoskeletal geometry between cells. We discuss the link between cadherin-complex dynamics and the actomyosin cytoskeleton at asymmetric cell-cell junctions. We then outline the role of Bin/Amphiphysin/Rvs (BAR) proteins, cytoplasmic regulators of endocytosis and cytoskeletal dynamics that sense force-induced membrane curvature, at AJs undergoing asymmetric remodeling. Lastly, we highlight the physiological importance of junctional asymmetry for epithelial and vascular tissue and discuss its potential role in disease.
Keywords: BAR domain; cadherin; collective cell migration; mechanotransduction; pacsin; polarity; tubular membrane.
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