Cell–cell and cell–matrix adhesions play essential roles in the function of tissues. There is growing evidence for the importance of cross talk between these two adhesion types, yet little is known about the impact of these interactions on the mechanical coupling of cells to the extracellular matrix (ECM). Here, we combine experiment and theory to reveal how intercellular adhesions modulate forces transmitted to the ECM. In the absence of cadherin-based adhesions, primary mouse keratinocytes within a colony appear to act independently, with significant traction forces extending throughout the colony. In contrast, with strong cadherin-based adhesions, keratinocytes in a cohesive colony localize traction forces to the colony periphery. Through genetic or antibody-mediated loss of cadherin expression or function, we show that cadherin-based adhesions are essential for this mechanical cooperativity. A minimal physical model in which cell–cell adhesions modulate the physical cohesion between contractile cells is sufficient to recreate the spatial rearrangement of traction forces observed experimentally with varying strength of cadherin-based adhesions. This work defines the importance of cadherin-based cell–cell adhesions in coordinating mechanical activity of epithelial cells and has implications for the mechanical regulation of epithelial tissues during development, homeostasis, and disease.

To understand how the mechanical properties of tissues emerge from interactions of multiple cells, we measure traction stresses of cohesive colonies of 1–27 cells adherent to soft substrates. We find that traction stresses are generally localized at the periphery of the colony and the total traction force scales with the colony radius. For large colony sizes, the scaling appears to approach linear, suggesting the emergence of an apparent surface tension of the order of ${10}^{-3}\mathrm{N}/\mathrm{m}$. A simple model of the cell colony as a contractile elastic medium coupled to the substrate captures the spatial distribution of traction forces and the scaling of traction forces with the colony size.

Actin is the main protein used by biological cells to adapt their structure and mechanics to their needs. Cellular adaptation is made possible by molecular processes that strongly depend on mechanics. The actin cytoskeleton is also an active material that continuously consumes energy. This allows for dynamical processes that are possible only out of equilibrium and opens up the possibility for multiple layers of control that have evolved around this single protein. Here we discuss the actin cytoskeleton from the viewpoint of physics as an active adaptive material that can build structures superior to man-made soft matter systems. Not only can actin be used to build different network architectures on demand and in an adaptive manner, but it also exhibits the dynamical properties of feedback systems, like excitability, bistability, or oscillations. Therefore, it is a prime example of how biology couples physical structure and information flow and a role model for biology-inspired metamaterials.