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Spatiotemporal patterns in multicellular systems are important to understanding tissue dynamics, for instance, during embryonic development and disease. Here, we use a multiphase field model to study numerically the behavior of a near-confluent monolayer of deformable cells with intercellular friction. Varying friction and cell motility drives a solid–liquid transition, and near the transition boundary, we find the emergence of local nematic order of cell deformation driven by shear-aligning cellular flows. Intercellular friction contributes to the monolayer’s viscosity, which significantly increases the spatial correlation in the flow and, concomitantly, the extent of nematic order. We also show that local hexatic and nematic order are tightly coupled and propose a mechanical-geometric model for the colocalization of $+1/2$nematic defects and 5–7 disclination pairs, which are the structural defects in the hexatic phase. Such topological defects coincide with regions of high cell–cell overlap, suggesting that they may mediate cellular extrusion from the monolayer, as found experimentally. Our results delineate a mechanical basis for the recent observation of nematic and hexatic order in multicellular collectives in experiments and simulations and pinpoint a generic pathway to couple topological and physical effects in these systems. 

Multiphase field models have emerged as an important computational tool for understanding biological tissue while resolving single-cell properties. While they have successfully reproduced many experimentally observed behaviors of living tissue, the theoretical underpinnings have not been fully explored. We show that a two-dimensional version of the model, which is commonly employed to study tissue monolayers, can be derived from a three-dimensional version in the presence of a substrate. We also show how viscous forces, which arise from friction between different cells, can be included in the model. Finally, we numerically simulate a tissue monolayer and find that intercellular friction tends to solidify the tissue. Published by the American Physical Society2024 

Using a multi-phase field model, we examine how cell stiffness affects motility induced phase separation (MIPS). 

Abstract Active processes drive biological dynamics across various scales and include subcellular cytoskeletal remodelling, tissue development in embryogenesis and the population-level expansion of bacterial colonies. In each of these, biological functionality requires collective flows to occur while self-organised structures are protected. However, the mechanisms by which active flows can spontaneously constrain their dynamics to preserve structure are not known. Here, by studying collective flows and defect dynamics in active nematic films, we demonstrate the existence of a self-constraint, namely a two-way, spontaneously arising relationship between activity-driven isosurfaces of flow boundaries and mesoscale nematic structures. We show that self-motile defects are tightly constrained to viscometric surfaces, which are contours along which the vorticity and the strain rate are balanced. This in turn reveals that self-motile defects break mirror symmetry when they move along a single viscometric surface. This is explained by an interdependence between viscometric surfaces and bend walls, which are elongated narrow kinks in the orientation field. These findings indicate that defects cannot be treated as solitary points. Instead, their associated mesoscale deformations are key to the steady-state coupling to hydrodynamic flows. This mesoscale cross-field self-constraint offers a framework for tackling complex three-dimensional active turbulence, designing dynamic control into biomimetic materials and understanding how biological systems can employ active stress for dynamic self-organisation.