Cell protrusions and contractions generate long-range membrane tension propagation.

Membrane tension is thought to be a long-range integrator of cell physiology. Membrane tension has been proposed to enable cell polarity during migration through front-back coordination and long-range protrusion competition. These roles necessitate effective tension transmission across the cell. However, conflicting observations have left the field divided as to whether cell membranes support or resist tension propagation. This discrepancy likely originates from the use of exogenous forces that may not accurately mimic endogenous forces. We overcome this complication by leveraging optogenetics to directly control localized actin-based protrusions or actomyosin contractions while simultaneously monitoring the propagation of membrane tension using dual-trap optical tweezers. Surprisingly, actin-driven protrusions and actomyosin contractions both elicit rapid global membrane tension propagation, whereas forces applied to cell membranes alone do not. We present a simple unifying mechanical model in which mechanical forces that engage the actin cortex drive rapid, robust membrane tension propagation through long-range membrane flows.

Rigidity-Controlled Crossover: From Spinodal to Critical Failure.

Failure in disordered solids is accompanied by intermittent fluctuations extending over a broad range of scales. The implied scaling has been previously associated with either spinodal or critical points. We use an analytically transparent mean-field model to show that both analogies are relevant near the brittle-to-ductile transition. Our study indicates that in addition to the strength of quenched disorder, an appropriately chosen global measure of rigidity (connectivity) can be also used to tune the system to criticality. By interpreting rigidity as a timelike variable we reveal an intriguing parallel between earthquake-type critical failure and Burgers turbulence.

Functionality of Disorder in Muscle Mechanics.

A salient feature of skeletal muscles is their ability to take up an applied slack in a microsecond timescale. Behind this fast adaptation is a collective folding in a bundle of elastically interacting bistable elements. Since this interaction has a long-range character, the behavior of the system in force and length controlled ensembles is different; in particular, it can have two distinct order-disorder-type critical points. We show that the account of the disregistry between myosin and actin filaments places the elementary force-producing units of skeletal muscles close to both such critical points. The ensuing "double criticality" contributes to the system's ability to perform robustly and suggests that the disregistry is functional.