Inelastic mechanics of biopolymer networks and cells

I use an integrated approach of experiments, theory, and numerical evaluations to show that stiffening and softening/fluidization are natural consequences of the assumption that the cytoskeleton is mechanically essentially equivalent to a transiently crosslinked biopolymer network. I perform experiments on in vitro reconstituted actin/HMM networks and show that already these simple, inanimate systems display fludization and shake-down, but at the same time stress stiffening. Based on the well-established Wlc theory, I then develop a semi-phenomenological mean-field model of a transiently crosslinked biopolymer network, which I call the inelastic glassy wormlike chain (inelastic Gwlc). At the heart of the model is the nonlinear interplay between viscoelastic single-polymer stiffening and inelastic softening by bond breaking. The model predictions are in good agreement with the actin/HMM experiments. Despite of its simplicity, the inelastic Gwlc model displays a rich phenomenology. It reproduces the hallmarks of the mechanics of adherent cells such as power-law rheology, stress and strain stiffening, kinematic hardening, shake-down, fludization, and recovery. The model also may also be able to provide considerable theoretical insights into the underlying physics. For example, using the inelastic Gwlc model, I am able to resolve the apparent paradox between cell softening and stiffening in terms of a parameter-dependent competition of antagonistic nonlinear microscopic mechanisms. I further shed light on the mechanism responsible for fluidization. I identify pertinent parameters characterizing the microstructure and give criteria for the relevance of various effects, including the effect of catch-bonds on the network response. Finally, a way to incorporate irreversible plastic flow is proposed