Abstract
The differential elastic modulus of an active actomyosin network is computed as a function of applied stress, taking into account both thermal and motor contributions to filament compliance in the low-frequency domain. It is shown that, due to a dual nature of motor activity, increasing motor concentration may either stiffen the network due to stronger prestress or soften it due to motor agitation, in accordance with experimental data. Prestress anisotropy, which may be induced by redistribution of motors triggered by external force, causes anisotropy of the elastic moduli. This helps to explain the contradictory phenomena of cell fluidization and resolidification in response to transient stretch observed in recent experiments.
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