Plasticity induced by active force dipoles: a defect-driven transition?

Experiments in composites of passive actin filaments and microtubule-motor assemblies show activity-driven flow that can transition from being extensile to contractile (Berezney et .al., PNAS (2022)). In Strubing et. al., Nano Lett. (2020), there was also a clear indication of plasticity in the network, accompanying this transition. In this talk, we will present results from a minimal model of a polymer network driven by active-force dipoles. Such networks are known to exhibit amplification and rectification of active stresses. We have shown that the origin of rectification is collective buckling at large scales. This effect also renormalizes the elastic modulii of the network creating a highly anisotropic one. In a variation of the model where we allow the network components to yield beyond a threshold stress, active force dipoles lead to plastic failure of the originally rigid network. Precisely, beyond a certain density of active force dipole, the network exhibits a transition from an elastic response to one characteristic of plasticity in amorphous solids. The "defects" leading to plasticity are "stress- defects" rather than geometric ones. Force dipoles have recently been mapped to tear-defects in thin sheets (Manoj et. al. PRL (2021)). We will exploit this mapping to analyze whether activity-driven plasticity can be understood as a phase transition driven by defects or as a manifestation of rigidity percolation.