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The accumulation and transmission of mechanical stresses in the cell cortex and membrane determines the mechanics of cell shape and coordinates essential physical behaviors, from cell polarization to cell migration. However, the extent that the membrane and cytoskeleton each contribute to the transmission of mechanical stresses to coordinate diverse behaviors is unclear. Here, we reconstitute a minimal model of the actomyosin cortex within liposomes that adheres, spreads and ultimately ruptures on a surface. During spreading, accumulated adhesion-induced (passive) stresses within the membrane drive changes in the spatial assembly of actin. By contrast, during rupture, accumulated myosin-induced (active) stresses within the cortex determine the rate of pore opening. Thus, in the same system, devoid of biochemical regulation, the membrane and cortex can each play a passive or active role in the generation and transmission of mechanical stress, and their relative roles drive diverse biomimetic physical behaviors.

 

We investigate the structural, vibrational, and mechanical properties of jammed packings of deformable particles with shape degrees of freedom in three dimensions (3D). Each 3D deformable particle is modeled as a surface-triangulated polyhedron, with spherical vertices whose positions are determined by a shape-energy function with terms that constrain the particle surface area, volume, and curvature, and prevent interparticle overlap. We show that jammed packings of deformable particles without bending energy possess low-frequency, quartic vibrational modes, whose number decreases with increasing asphericity and matches the number of missing contacts relative to the isostatic value. In contrast, jammed packings of deformable particles with non-zero bending energy are isostatic in 3D, with no quartic modes. We find that the contributions to the eigenmodes of the dynamical matrix from the shape degrees of freedom are significant over the full range of frequency and shape parameters for particles with zero bending energy. We further show that the ensemble-averaged shear modulus 〈 G 〉 scales with pressure P as 〈 G 〉 ∼ P β , with β ≈ 0.75 for jammed packings of deformable particles with zero bending energy. In contrast, β ≈ 0.5 for packings of deformable particles with non-zero bending energy, which matches the value for jammed packings of soft, spherical particles with fixed shape. These studies underscore the importance of incorporating particle deformability and shape change when modeling the properties of jammed soft materials. 

Living and non-living active matter consumes energy at the microscopic scale to drive emergent, macroscopic behavior including traveling waves and coherent oscillations. Recent work has characterized non-equilibrium systems by their total energy dissipation, but little has been said about how dissipation manifests in distinct spatiotemporal patterns. We introduce a measure of irreversibility we term the entropy production factor to quantify how time reversal symmetry is broken in field theories across scales. We use this scalar, dimensionless function to characterize a dynamical phase transition in simulations of the Brusselator, a prototypical biochemically motivated non-linear oscillator. We measure the total energetic cost of establishing synchronized biochemical oscillations while simultaneously quantifying the distribution of irreversibility across spatiotemporal frequencies.

 

Unlike nearly all engineered materials which contain bonds that weaken under load, biological materials contain “catch” bonds which are reinforced under load. Consequently, materials, such as the cell cytoskeleton, can adapt their mechanical properties in response to their state of internal, non‐equilibrium (active) stress. However, how large‐scale material properties vary with the distance from equilibrium is unknown, as are the relative roles of active stress and binding kinetics in establishing this distance. Through course‐grained molecular dynamics simulations, the effect of breaking of detailed balance by catch bonds on the accumulation and dissipation of energy within a model of the actomyosin cytoskeleton is explored. It is found that the extent to which detailed balance is broken uniquely determines a large‐scale fluid‐solid transition with characteristic time‐reversal symmetries. The transition depends critically on the strength of the catch bond, suggesting that active stress is necessary but insufficient to mount an adaptive mechanical response.

 

During intracellular transport, cellular cargos, such as organelles, vesicles, and proteins, are transported within cells. Intracellular transport plays an important role in diverse cellular functions. Molecular motors walking on the cytoskeleton facilitate active intracellular transport, which is more efficient than diffusion‐based passive transport. Active transport driven by kinesin and dynein walking on microtubules has been studied well during recent decades. However, mechanisms of active transport occurring in disorganized actin networks via myosin motors remain elusive. To provide physiologically relevant insights, we probed motions of myosin motors in actin networks under various conditions using our well‐established computational model that rigorously accounts for the mechanical and dynamical behaviors of the actin cytoskeleton. We demonstrated that myosin motions can be confined due to three different reasons in the absence of F‐actin turnover. We verified mechanisms of motor stalling using in vitro reconstituted actomyosin networks. We also found that with F‐actin turnover, motors consistently move for a long time without significant confinement. Our study sheds light on the importance of F‐actin turnover for effective active transport in the actin cytoskeleton.