Geometrical origins of contractility in disordered actomyosin networks

TL;DR

This paper presents a geometric model explaining how disordered actomyosin networks favor contraction over extension, revealing a dominant mechanism where motors transverse actin filaments to generate contractile forces.

Contribution

The study introduces a mathematical framework identifying a primary contraction mechanism in disordered actomyosin networks, emphasizing the role of transverse filament deformation.

Findings

Transverse filament deformation dominates contractility.

A specific geometric mechanism explains force generation.

Model aligns with recent in vitro experiments.

Abstract

Movement within eukaryotic cells largely originates from localized forces exerted by myosin motors on scaffolds of actin filaments. Although individual motors locally exert both contractile and extensile forces, large actomyosin structures at the cellular scale are overwhelmingly contractile, suggesting that the scaffold serves to favor contraction over extension. While this mechanism is well understood in highly organized striated muscle, its origin in disordered networks such as the cell cortex is unknown. Here we develop a mathematical model of the actin scaffold's local two- or three-dimensional mechanics and identify four competing contraction mechanisms. We predict that one mechanism dominates, whereby local deformations of the actin break the balance between contraction and extension. In this mechanism, contractile forces result mostly from motors plucking the filaments transversely rather than buckling them longitudinally. These findings sheds light on recent $\textit{in vitro}$ experiments, and provides a new geometrical understanding of contractility in the myriad of disordered actomyosin systems found $\textit{in vivo}$.