We consider chirality in active systems by exemplarily studying the phase behavior of planar systems of interacting Brownian circle swimmers with a spherical shape. For this purpose, we derive a predictive field theory that is able to describe the collective dynamics of circle swimmers. The theory yields a mapping between circle swimmers and noncircling active Brownian particles and predicts that the angular propulsion of the particles leads to a suppression of their motility-induced phase separation, being in line with recent simulation results. In addition, the theory provides analytical expressions for the spinodal corresponding to the onset of motility-induced phase separation and the associated critical point as well as for their dependence on the angular propulsion of the circle swimmers. We confirm our findings by Brownian dynamics simulations. The agreement between results from theory and simulations is found to be good.

We investigate the influence of external forces on the collective dynamics of interacting active Brownian particles in two as well as three spatial dimensions. Via explicit coarse graining, we derive predictive models that are applicable for space-and time-dependent external force fields. We study these models for the cases of gravity and harmonic traps. In particular, we derive a generalized barometric formula for interacting active Brownian particles under gravity that is valid for low to high concentrations and activities of the particles. Furthermore, we show that one can use an external harmonic trap to induce motility-induced phase separation in systems that, without external fields, remain in a homogeneous state. This finding makes it possible to realize programmable density patterns in systems of active Brownian particles. Our analytic predictions are found to be in very good agreement with Brownian dynamics simulations.

A key behavior observed during morphogenesis, wound healing, and cancer invasion is that of collective and coordinated cellular motion. Hence, understanding the different aspects of such coordinated migration is fundamental for describing and treating cancer and other pathological defects. In general, individual cells exert forces on their environment in order to move, and collective motion is coordinated by cell–cell adhesion‐based forces. However, this notion ignores other mechanisms that encourage cellular movement, such as pressure differences. Here, using model tumors, it is found that increased pressure drove coordinated cellular motion independent of cell–cell adhesion by triggering cell swelling in a soft extracellular matrix (ECM). In the resulting phenotype, a rapid burst‐like stream of cervical cancer cells emerged from 3D aggregates embedded in soft collagen matrices (0.5 mg mL−1). This fluid‐like pushing mechanism, recorded within 8 h after embedding, shows high cell velocities and super‐diffusive motion. Because the swelling in this model system critically depends on integrin‐mediated cell–ECM adhesions and cellular contractility, the swelling is likely triggered by unsustained mechanotransduction, providing new evidence that pressure‐driven effects must be considered to more completely understand the mechanical forces involved in cell and tissue movement as well as invasion.

Collective migration of cells is a key behaviour observed during morphogenesis, wound healing and cancer cell invasion. Hence, understanding the different aspects of collective migration is at the core of further progress in describing and treating cancer and other pathological defects. The standard dogma in cell migration is that cells exert forces on the environment to move and cell-cell adhesion-based forces provide the coordination for collective migration. Here, we report a new collective migration mechanism that is independent of pulling forces on the extra-cellular matrix (ECM), as it is driven by the pressure difference generated inside model tumours. We observe a striking collective migration phenotype, where a rapid burst-like stream of HeLa cervical cancer cells emerges from the 3D aggregate embedded in matrices with low collagen concentration (0.5 mg ml−1). This invasion-like behaviour is recorded within 8 hours post embedding (hpe), and is characterised by high cell velocity and super-diffusive collective motion. We show that cellular swelling, triggered by the soft matrix, leads to a rise in intrinsic pressure, which eventually drives an invasion-like phenotype of HeLa cancer aggregates. These dynamic observations provide new evidence that pressure-driven effects need to be considered for a complete description of the mechanical forces involved in collective migration and invasion.