| Summary: | The magnitude of mechanical stresses caused by cell surface tension may be comparable to the bulk elasticity of their matrix on cellular length scales, yet how capillary effects influence tissue shape and motion are unknown. In this work, we induce wetting (spreading and migration) of cell aggregates, as models of active droplets onto adhesive substrates of varying elasticity, and correlate the dynamics of wetting to the balance of interfacial tensions. Upon wetting rigid substrates, cell-substrate tension drives outward expansion of the monolayer. By contrast, upon wetting compliant substrates, cell-substrate tension is attenuated and aggregate capillary forces contribute to internal pressures that drive expansion. Thus, we show by experiments, data-driven modeling, and computational simulations that myosin-driven “active elastocapillary” effects enable adaptation of wetting mechanisms to substrate rigidity and introduce a novel, pressure-based mechanism for guiding collective cell motion.
|
|---|