The slip instability of an earthquake and its abrupt energy release depend primarily on the intensity of strength drop during accelerated fault slip. This process is typically attributed to changes of frictional resistance between two sliding blocks. Here we show that friction changes alone cannot explain observed strength variations of artificial fault zones. Sandstone samples with saw-cut faults and gypsum gouge zones were subjected to many cycles of hold-slide loading. Samples with water-saturated gouge display (1) systematic, time-dependent increase of gouge strength; (2) unstable failure of gouge with large stress drops; and (3) lithification of gouge by crack sealing, recrystallization, porosity reduction, and grain bonding. All these features are absent in identical tests with dry gouge. These observations indicate that gouge particles are cemented by chemical processes during hold periods and suggest that the cyclical strength variations are controlled by cohesion strengthening rather than by friction changes. We further hypothesize that crustal fault zones could be lithified during the interseismic stage, and this lithification would control earthquake-slip instability.

Recent experiments have demonstrated that dynein motors exhibit catch bonding behavior, in which the unbinding rate of a single dynein decreases with increasing force, for a certain range of force. Motivated by these experiments, we study the effect of catch bonding on unidirectional transport properties of cellular cargo carried by multiple dynein motors. We introduce a threshold force bond deformation (TFBD) model, consistent with the experiments, wherein catch bonding sets in beyond a critical applied load force. We find catch bonding can result in dramatic changes in the transport properties, which are in sharp contrast to kinesin-driven unidirectional transport, where catch bonding is absent. We predict that under certain conditions, the average velocity of the cellular cargo can actually increase as applied load is increased. We characterize the transport properties in terms of a velocity profile plot in the parameter space of the catch bond strength and the stall force of the motor. This plot yields predictions that may be experimentally accessed by suitable modifications of motor transport and binding properties.

We introduce a multispecies lattice-gas model for motor protein driven collective cargo transport on cellular filaments. We use this model to describe and analyze the collective motion of interacting vesicle cargos being carried by oppositely directed molecular motors, moving on a single biofilament. Building on a totally asymmetric exclusion process to characterize the motion of the interacting cargos, we allow for mass exchange with the environment, input, and output at filament boundaries and focus on the role of interconversion rates and how they affect the directionality of the net cargo transport. We quantify the effect of the various different competing processes in terms of nonequilibrium phase diagrams. The interplay of interconversion rates, which allow for flux reversal and evaporation-deposition processes, introduces qualitatively unique features in the phase diagrams. We observe regimes of three-phase coexistence, the possibility of phase re-entrance, and a significant flexibility in how the different phase boundaries shift in response to changes in control parameters. The moving steady-state solutions of this model allows for different possibilities for the spatial distribution of cargo vesicles, ranging from homogeneous distribution of vesicles to polarized distributions, characterized by inhomogeneities or shocks. Current reversals due to internal regulation emerge naturally within the framework of this model. We believe that this minimal model will clarify the understanding of many features of collective vesicle transport, apart from serving as the basis for building more exact quantitative models for vesicle transport relevant to various in vivo situations.

We study a minimal lattice model which describes bidirectional transport of "particles" driven along a one-dimensional track, as is observed in microtubule based, motor protein driven bidirectional transport of cargo vesicles, lipid bodies, and organelles such as mitochondria. This minimal model, a multispecies totally asymmetric exclusion process (TASEP) with directional switching, can provide a framework for understanding the interplay between the switching dynamics of individual particles and the collective movement of particles in one dimension. When switching is much faster than translocation, the steady-state density and current profiles of the particles are homogeneous in the bulk and are well described by mean-field (MF) theory, as determined by comparison to a Monte Carlo simulation. In this limit, we can map this model to the exactly solvable partially asymmetric exclusion-process (PASEP) model. Away from this fast switching regime the MF theory fails, although the average bulk density profile still remains homogeneous. We study the steady-state behavior as a function of the ratio of the translocation and net switching rates Q and find a unique first-order phase transition at a finite Q associated with a discontinuous change of the bulk density. When the switching rate is decreased further (keeping translocation rate fixed), the system approaches a jammed phase with a net current that tends to zero as J~1/Q. We numerically construct the phase diagram for finite Q.