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By modelling epithelial cells as active nematic liquid crystals, stresses induced at the sites of topological defects are found to be the primary drivers of extrusion and cell death.

Epithelial wound closure proceeds through both crawling into the wound and by constricting an actomyosin cable in a so-called purse-string mechanism. Here the authors show that the two mechanisms are mechanically coupled and the curvature of the wound regulates the overall dynamics of wound closure.

On soft substrates, epithelial tissues are under high tension and form holes that spontaneously heal. Thus, mechanical stress directly impacts the integrity of epithelia.

Cells can modify their environment by depositing biochemical signals or mechanically remodelling the extracellular matrix; the impact of such self-induced environmental perturbations on cell trajectories at various scales remains unexplored. Here authors show that motile cells leave long-lived physicochemical footprints along their way, which determine their future path.

Cell extrusion regulates monolayer cell density and is critical in maintaining epithelia integrity, which has implications in homeostasis, development, and cancer progression. Here the authors describe how monolayer integrate mechanical signals from tissue mechanics, cell-cell adhesion, cell-substrate adhesion and cytoskeleton coordinate cell extrusion.

Collective cell migration is usually attributed to large-scale transmission of signals through cell junctions. Here, the authors confine cells into a ring-shaped pattern and show that collective cell migration can arise at the single-cell level.

During migration, cells interact with their environment by exerting mechanical forces on it. A combination of two techniques shows that they do so in all three dimensions by a push–pull mechanism.

The formation of complex organs, tissue repair and metastasis all require a coordinated regulation of the shape and movement of groups of cells. The mechanical means of communication between cells is crucial to understanding collective cell motions — so how can cells transmit physical forces within cell sheets?

Closure of epithelial gaps such as wounds is thought to involve contraction of an actomyosin ‘purse-string’. By creating non-adherent gaps to exclude contributions of adhesive protrusion, the authors find that large-scale tension, more than purse-string contraction, mediates closure.

Adherent cells actively probe the rigidity of their substrates. Guptaet al. show that actin cytoskeleton rheology transitions from fluid to solid with increased substrate stiffness along with an isotropic to nematic ordering, implicating the remodelling of the whole actin network in rigidity sensing.

It is now revealed, using cell cultures and in silico models, that weakening intercellular contacts is a fundamental process essential for switching from extensile to contractile tissue behaviour.

Changes in membrane curvature influence how migrating cells navigate their environment. Experiments and modelling reveal that dynamic reorganization of the actin cytoskeleton in response to these changes provides cells with a sensing mechanism.

Collective epithelial behaviours are studied in vitro in the context of flat sheets but a system to mimic tubular systems is lacking. Here, the authors develop a method to study collective behaviour in lumenal structures and show that several features depend on the extent of tubular confinement and/or curvature.

Wound repair is thought to involve cell migration and the contraction of a tissue-level biopolymer ring—invoking analogy with the pulling of purse strings. Traction-force measurements now show that this ring engages the tissue's surroundings to steer migration, prompting revision of the purse-string mechanism.

In wound healing, skin cells collectively migrate to maintain tissue cohesion despite the existence of inhomogeneities in the extracellular environment within the wound bed. Yet how the cell collective responds to heterogeneities in the extracellular matrix is not well understood. Now, it is shown that migrating human keratinocyte cell sheets form suspended multicellular bridges over non-adhesive regions on micropatterned substrates comprising alternating strips of fibronectin and non-adherent polymer.

Coordinated movements of cell collectives are important for morphogenesis, tissue regeneration and cancer cell dissemination. Recent studies, mainly using novelin vitroapproaches, have provided new insights into the mechanisms governing this multicellular coordination, highlighting the key role of the mechanosensitivity of adherens junctions and mechanical cell–cell coupling in collective cell behaviours.

A class of biological matter including elongated cells and filaments can be understood in the framework of active nematic liquid crystals. Within these systems, topological defects emerge and give rise to remarkable collective behaviours.

The dynamics of epithelial tissues play a key role in tissue organization, both in health and disease. In this Review, the authors discuss materials and techniques for the study of epithelial movement and mechanics and investigate epithelia as active matter from a theoretical and experimental perspective.