Epithelial monolayers remove excess cells by extrusion. Benoit Ladoux and colleagues now report a purely mechanical route to cell extrusion at the site of topological defects within the cell monolayer. By modelling the epithelium as an active nematic liquid crystal, they show that cell extrusion is driven by stresses induced by distortions in cell orientation. Extrusion hotspots were controlled by geometrically inducing defects through microcontact printing of patterned monolayers. The authors also investigated the mechanotransductive effect of stress localization and found that signals related to cell death were induced at these sites of compressive stress. Additionally, tampering with the intercellular adhesion complexes led to a weakening of cell–cell interactions and resulted in an increased number of defects and extrusions. This finding is in line with nematic theory, which predicts that the number of topological defects is inversely related to the orientational elasticity.
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