Fluidization and Active Thinning by Molecular Kinetics in Active Gels

TL;DR

This paper develops a molecular-level model for active gels, revealing how molecular kinetics induce fluidization, active stresses, and active thinning, with implications for understanding cell mechanics.

Contribution

It introduces a molecular-based constitutive model linking molecular kinetics to active gel rheology, including explicit transport coefficients and predictions of active thinning.

Findings

Molecular binding kinetics induce Maxwell viscoelasticity.

Active stresses arise when detailed balance is broken.

Active thinning occurs when activity promotes linker unbinding.

Abstract

We derive the constitutive equations of an active polar gel from a model for the dynamics of elastic molecules that link polar elements. Molecular binding kinetics induces the fluidization of the material, giving rise to Maxwell viscoelasticity and, provided that detailed balance is broken, to the generation of active stresses. We give explicit expressions for the transport coefficients of active gels in terms of molecular properties, including nonlinear contributions on the departure from equilibrium. In particular, when activity favors linker unbinding, we predict a decrease of viscosity with activity - active thinning - of kinetic origin, which could explain some experimental results on the cell cortex. By bridging the molecular and hydrodynamic scales, our results could help understand the interplay between molecular perturbations and the mechanics of cells and tissues.