Force-velocity correlations in a dense, collisional, granular flow

We report measurements in a 2-dimensional, gravity-driven, collisional, granular flow of the normal force delivered to the wall and of particle velocity at several points in the flow. The wall force and the flow velocity are negatively correlated. This correlation falls off only slowly with distance transverse to the flow, but dies away on the scale of a few particle diameters upstream or downstream. The data support a picture of short-lived chains of frequently colliding particles that extend transverse to the flow direction, making transient load-bearing bridges that cause bulk fluctuations in the flow velocity. The time-dependence of these spatial correlation functions indicate that while the force-bearing structures are local in space, their influence extends far upstream in the flow, albeit with a time-lag. This leads to correlated velocity fluctuations, whose spatial range increases as the jamming threshold is approached.Comment: to be submitted for publicatio

Requirements for contractility in disordered cytoskeletal bundles

Actomyosin contractility is essential for biological force generation, and is well understood in highly organized structures such as striated muscle. Additionally, actomyosin bundles devoid of this organization are known to contract both in vivo and in vitro, which cannot be described by standard muscle models. To narrow down the search for possible contraction mechanisms in these systems, we investigate their microscopic symmetries. We show that contractile behavior requires non-identical motors that generate large enough forces to probe the nonlinear elastic behavior of F-actin. This suggests a role for filament buckling in the contraction of these bundles, consistent with recent experimental results on reconstituted actomyosin bundles.Comment: 10 pages, 6 figures; text shortene

Contractile units in disordered actomyosin bundles arise from F-actin buckling

Bundles of filaments and motors are central to contractility in cells. The classic example is striated muscle, where actomyosin contractility is mediated by highly organized sarcomeres which act as fundamental contractile units. However, many contractile bundles in vivo and in vitro lack sarcomeric organization. Here we propose a model for how contractility can arise in actomyosin bundles without sarcomeric organization and validate its predictions with experiments on a reconstituted system. In the model, internal stresses in frustrated arrangements of motors with diverse velocities cause filaments to buckle, leading to overall shortening. We describe the onset of buckling in the presence of stochastic actin-myosin detachment and predict that buckling-induced contraction occurs in an intermediate range of motor densities. We then calculate the size of the "contractile units" associated with this process. Consistent with these results, our reconstituted actomyosin bundles contract at relatively high motor density, and we observe buckling at the predicted length scale.Comment: 5 pages, 4 figures, Supporting text and movies attache