  The mechanical properties of cells are dominated by the cytoskeleton, an
interconnected network of long elastic filaments. The connections between the
filaments are provided by crosslinking proteins, which constitute, next to the
filaments, the second important mechanical element of the network. An important
aspect of cytoskeletal assemblies is their dynamic nature, which allows
remodeling in response to external cues. The reversible nature of crosslink
binding is an important mechanism that underlies these dynamical processes.
Here, we develop a theoretical model that provides insight into how the
mechanical properties of cytoskeletal networks may depend on their underlying
constituting elements. We incorporate three important ingredients: nonaffine
filament deformations in response to network strain; interplay between filament
and crosslink mechanical properties; reversible crosslink (un)binding in
response to imposed stress. With this we are able to self-consistently
calculate the nonlinear modulus of the network as a function of deformation
amplitude and crosslink as well as filament stiffnesses. During loading
crosslink unbinding processes lead to a relaxation of stress and therefore to a
reduction of the network modulus and eventually to network failure, when all
crosslink are unbound. This softening due to crosslink unbinding generically
competes with an inherent stiffening response, which may either be due to
filament or crosslink nonlinear elasticity.
