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.

a b s t r a c tThe rate-and-state formulation of friction is well established as a phenomenological yet quantitative description of friction dynamics, in particular the onset of stick-slip instabilities arising from an oscillatory bifurcation. We first discuss the physical origins of two theories for the derivation of friction coefficients used in rate-and-state models, both derived from thermally activated rate processes. Secondly, we propose a general expression for the state evolution law in the form of a first order kinetics which describes the relaxation to a velocity dependent equilibrium interfacial state f ss ðvÞ over a velocity dependent dynamic rejuvenation time-scale t f ðvÞ. We show that the unknown relation f ss ðvÞ, defined as the ratio of t f to a constant interfacial stationary healing time-scale t ÃÃ , can be estimated directly from the experimental measurements of the steady-state friction coefficient and the critical stiffness for the onset of stick-slip behaviour of a spring-block system. Using a specific experimental dataset, we finally illustrate that this method provides the experimental measurements of the apparent memory length L a ðvÞ ¼ v t ÃÃ f ss ðvÞ and the constant characteristic relaxation time t ÃÃ from which a constant intrinsic memory length L ¼ V Ã t ÃÃ can be defined once a slip rate of reference V Ã is chosen. As a result the complete state evolution law can be experimentally characterised.

Motility initiation in crawling cells requires transformation of a symmetric state into a polarized state. In contrast, motility arrest is associated with re-symmetrization of the internal configuration of a cell. Experiments on keratocytes suggest that polarization is triggered by the increased contractility of motor proteins but the conditions of re-symmetrization remain unknown. In this paper we show that if adhesion with the extra-cellular substrate is sufficiently low, the progressive intensification of motor-induced contraction may be responsible for both transitions: from static (symmetric) to motile (polarized) at a lower contractility threshold and from motile (polarized) back to static (symmetric) at a higher contractility threshold. Our model of lamellipodial cell motility is based on a 1D projection of the complex intra-cellular dynamics on the direction of locomotion. In the interest of analytical transparency we also neglect active protrusion and view adhesion as passive. Despite the unavoidable oversimplifications associated with these assumptions, the model reproduces quantitatively the motility initiation pattern in fish keratocytes and reveals a crucial role played in cell motility by the nonlocal feedback between the mechanics and the transport of active agents. A prediction of the model that a crawling cell can stop and re-symmetrize when contractility increases sufficiently far beyond the motility initiation threshold still awaits experimental verification.

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.

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Structural vibration controlled by interfacial friction is widespread, ranging from friction dampers in gas turbines to the motion of violin strings. To predict, control or prevent such vibration, a constitutive description of frictional interactions is inevitably required. A variety of friction models are discussed to assess their scope and validity, in the light of constraints provided by different experimental observations. Three contrasting case studies are used to illustrate how predicted behaviour can be extremely sensitive to the choice of frictional constitutive model, and to explore possible experimental paths to discriminate between and calibrate dynamic friction models over the full parameter range needed for real applications.

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An earthquake is commonly described as a stick-slip frictional instability occurring along preexisting crustal faults. The seismic cycle of earthquake recurrence is characterised by long periods of quasi-static evolution which precede sudden slip events accompanied by elastic wave radiation: the earthquake. This succession of processes over two well distinguished time scales recalls the behaviour of nonlinear relaxation oscillations. We explore this connection by studying, in the framework of rate-and-state friction, the sliding of two identical slabs of elastic solid driven in opposite directions with a constant relative velocity. Our first innovation is to establish that the motion of a spring-block system is an asymptotic mechanical analogue of the frictional sliding of a single interface from which elastic waves radiate. Due to wave reflection at the boundaries, the equivalent mass of the block M = k(h/cs) 2 /12 is not independent of the equivalent spring stiffness k, where h denotes the slab thickness and cs is the shear wave speed. Considering a non-monotonic friction law, we show that the relaxation oscillation regime is reached when the characteristic time scale of frictionless oscillations is much greater than the characteristic time of frictional memory effects:L/V * . We combine a composite approximation of the stick-slip cycle and numerical studies to show that the interfacial relaxation oscillations result from the subtle interplay of the non-monotonic properties of the friction law driving the long stress build-up of the quasi-static phase, and the inertial control of the fast slip phase originating from the wave propagation. We discuss the geophysical consequences for earthquake mechanics, and connections between the rate-and-state and Coulomb models of friction.