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Tissues commonly consist of cells embedded within a fibrous biopolymer network. Whereas cell-free reconstituted biopolymer networks typically soften under applied uniaxial compression, various tissues, including liver, brain, and fat, have been observed to instead stiffen when compressed. The mechanism for this compression-stiffening effect is not yet clear. Here, we demonstrate that when a material composed of stiff inclusions embedded in a fibrous network is compressed, heterogeneous rearrangement of the inclusions can induce tension within the interstitial network, leading to a macroscopic crossover from an initial bending-dominated softening regime to a stretching-dominated stiffening regime, which occurs before and independently of jamming of the inclusions. Using a coarse-grained particle-network model, we first establish a phase diagram for compression-driven, stretching-dominated stress propagation and jamming in uniaxially compressed two- and three-dimensional systems. Then, we demonstrate that a more detailed computational model of stiff inclusions in a subisostatic semiflexible fiber network exhibits quantitative agreement with the predictions of our coarse-grained model as well as qualitative agreement with experiments.

 

Networks of filamentous actin (F-actin) are important for the mechanics of most animal cells. These cytoskeletal networks are highly dynamic, with a variety of actin-associated proteins that control cross-linking, polymerization and force generation in the cytoskeleton. Inspired by recent rheological experiments on reconstituted solutions of dynamic actin filaments, we report a theoretical model that describes stress relaxation behavior of these solutions in the presence of severing proteins. We show that depending on the kinetic rates of assembly, disassembly, and severing, one can observe both length-dependent and length-independent relaxation behavior. 

Hydrogels of semiflexible biopolymers such as collagen have been shown to contract axially under shear strain, in contrast to the axial dilation observed for most elastic materials. Recent work has shown that this behavior can be understood in terms of the porous, two-component nature and consequent time-dependent compressibility of hydrogels. The apparent normal stress measured by a torsional rheometer reflects only the tensile contribution of the axial component σ zz on long (compressible) timescales, crossing over to the first normal stress difference, N 1 = σ xx − σ zz at short (incompressible) times. While the behavior of N 1 is well understood for isotropic viscoelastic materials undergoing affine shear deformation, biopolymer networks are often anisotropic and deform nonaffinely. Here, we numerically study the normal stresses that arise under shear in subisostatic, athermal semiflexible polymer networks. We show that such systems exhibit strong deviations from affine behavior and that these anomalies are controlled by a rigidity transition as a function of strain.