Even the most regular stick-slip frictional sliding is always stochastic, with irregularity in both the intervals between slip events and the sizes of the associated stress drops. Applying small-amplitude oscillations to the shear force, we show, experimentally and theoretically, that the stick-slip periods synchronize. We further show that this phase locking is related to the inhibition of slow rupture modes which forces a transition to fast rupture, providing a possible mechanism for observed remote triggering of earthquakes. Such manipulation of collective modes may be generally relevant to extended nonlinear systems driven near to criticality.

Faults are intrinsically heterogeneous with common occurrences of jogs, edges and steps. We therefore explore experimentally and theoretically how fault edges may affect earthquake and slip dynamics. In the presented experiments and accompanying theoretical model, shear loads are applied to the edge of one of two flat blocks in frictional contact that form a fault analog. We show that slip occurs via a sequence of rapid rupture events that initiate from the loading edge and are arrested after propagating a finite distance. Each successive event extends the slip size, transfers the applied shear across the block, and causes progressively larger changes of the contact area along the contact surface. Resulting from this sequence of events, a hard asperity is dynamically formed near the loaded edge. The contact area beyond this asperity is largely reduced. These sequences of rapid events culminate in slow slip events that precede a major, unarrested slip event along the entire contact surface. We suggest that the 1998 M5.0 Sendai and 1995 off-Etorofu earthquake sequences may correspond to this scenario. Our work demonstrates, qualitatively, how the simplest deviation from uniform shear loading may significantly affect both earthquake nucleation processes and how fault complexity develops.

Bacillus subtilis is able to form architecturally complex biofilms on solid medium due to the production of an extracellular matrix. A master regulator that controls the expression of the genes involved in matrix synthesis is Spo0A, which is activated by phosphorylation via a phosphorelay involving multiple histidine kinases. Here we report that four kinases, KinA, KinB, KinC, and KinD, help govern biofilm formation but that their contributions are partially masked by redundancy. We show that the kinases fall into two categories and that the members of each pair (one pair comprising KinA and KinB and the other comprising KinC and KinD) are partially redundant with each other. We also show that the kinases are spatially regulated: KinA and KinB are active principally in the older, inner regions of the colony, and KinC and KinD function chiefly in the younger, outer regions. These conclusions are based on the morphology of kinase mutants, real-time measurements of gene expression using luciferase as a reporter, and confocal microscopy using a fluorescent protein as a reporter. Our findings suggest that multiple signals from the older and younger regions of the colony are integrated by the kinases to determine the overall architecture of the biofilm community.