Active gel segment behaving as an active particle.

We reduce a one-dimensional model of an active segment (AS), which is used, for instance, in the description of contraction-driven cell motility, to a zero-dimensional model of an active particle (AP) characterized by two internal degrees of freedom: position and polarity. Both models give rise to hysteretic force-velocity relations showing that an active agent can support two opposite polarities under the same external force and that it can maintain the same polarity while being dragged by external forces with opposite orientations. This double bistability results in a rich dynamic repertoire which we illustrate by studying static, stalled, motile, and periodically repolarizing regimes displayed by an active agent confined in a viscoelastic environment. We show that the AS and AP models can be calibrated to generate quantitatively similar dynamic responses.

Mechanical stress as a regulator of cell motility.

The motility of a cell can be triggered or inhibited not only by an applied force but also by a mechanically neutral force couple. This type of loading, represented by an applied stress and commonly interpreted as either squeezing or stretching, can originate from extrinsic interaction of a cell with its neighbors. To quantify the effect of applied stresses on cell motility we use an analytically transparent one-dimensional model accounting for active myosin contraction and induced actin turnover. We show that stretching can polarize static cells and initiate cell motility while squeezing can symmetrize and arrest moving cells. We show further that sufficiently strong squeezing can lead to the loss of cell integrity. The overall behavior of the system depends on the two dimensionless parameters characterizing internal driving (chemical activity) and external loading (applied stress). We construct a phase diagram in this parameter space distinguishing between static, motile, and collapsed states. The obtained results are relevant for the mechanical understanding of contact inhibition and the epithelial-to-mesenchymal transition.

A phase-plane analysis of localized frictional waves.

Sliding frictional interfaces at a range of length scales are observed to generate travelling waves; these are considered relevant, for example, to both earthquake ground surface movements and the performance of mechanical brakes and dampers. We propose an explanation of the origins of these waves through the study of an idealized mechanical model: a thin elastic plate subject to uniform shear stress held in frictional contact with a rigid flat surface. We construct a nonlinear wave equation for the deformation of the plate, and couple it to a spinodal rate-and-state friction law which leads to a mathematically well-posed problem that is capable of capturing many effects not accessible in a Coulomb friction model. Our model sustains a rich variety of solutions, including periodic stick-slip wave trains, isolated slip and stick pulses, and detachment and attachment fronts. Analytical and numerical bifurcation analysis is used to show how these states are organized in a two-parameter state diagram. We discuss briefly the possible physical interpretation of each of these states, and remark also that our spinodal friction law, though more complicated than other classical rate-and-state laws, is required in order to capture the full richness of wave types.

Contraction-driven cell motility.

We propose a mechanism for the initiation of cell motility that is based on myosin-induced contraction and does not require actin polymerization. The translocation of a cell is induced by symmetry breaking of the motor-driven flow, and the ensuing asymmetry gives rise to a steady motion of the center of mass of a cell. The predictions of the model are consistent with observations on keratocytes.