Actin based propulsion: Intriguing interplay between material properties and growth processes

Eukaryotic cells and intracellular pathogens such as bacteria or viruses utilize the actin polymerization machinery to propel themselves forward. Thereby, the onset of motion and choice of direction may be the result of a spontaneous symmetry-breaking or might be triggered by external signals and preexisting asymmetries, e.g. through a previous septation in bacteria. Although very complex, a key feature of cellular motility is the ability of actin to form dense polymeric networks, whose microstructure is tightly regulated by the cell. These polar actin networks produce the forces necessary for propulsion but may also be at the origin of a spontaneous symmetry-breaking. Understanding the exact role of actin dynamics in cell motility requires multiscale approaches which capture at the same time the polymer network structure and dynamics on the scale of a few nanometers and the macroscopic distribution of elastic stresses on the scale of the whole cell. In this chapter we review a selection of theories on how mechanical material properties and growth processes interact to induce the onset of actin based motion.

💡 Research Summary

The chapter provides a comprehensive review of how the mechanical material properties of actin networks interact with their growth processes to generate propulsion in eukaryotic cells and intracellular pathogens. It begins by outlining the biological context: actin polymerization drives the formation of dense, branched filamentous structures that generate the forces required for movement. The authors emphasize that the onset of motion can arise either spontaneously, through a symmetry‑breaking instability, or be triggered by external cues such as pre‑existing cellular asymmetries or bacterial septation.

A detailed theoretical background follows, describing the molecular players (Arp2/3 complex, formins, cofilin, profilin, capping proteins) that regulate filament nucleation, elongation, branching, and turnover. The balance between polymerization (k_on) and depolymerization (k_off) determines the volumetric growth rate of the network, which in turn creates internal elastic stresses that are highly non‑uniform because of the network’s anisotropic microstructure (branch density, filament orientation).

To capture these coupled phenomena, the authors present a multiscale modeling framework that merges continuum mechanics with stochastic filament‑level simulations. The continuum component treats the actin gel as a non‑Newtonian viscoelastic solid, linking macroscopic stress–strain relations to microscopic parameters such as branch density and filament length distribution. The stochastic component tracks individual filament events (addition, loss, branching, cross‑linking) using probabilistic rules derived from biochemical kinetics. By coupling the two, the framework demonstrates how microscopic noise can be amplified into a macroscopic symmetry‑breaking event: a slight local excess in filament length reduces local resistance, channels more polymer flux to that region, and triggers a positive feedback loop that rapidly polarizes the network.

Experimental validation is discussed through high‑resolution electron microscopy and fluorescence imaging of lamellipodia, “spiky” actin tails, and lead‑trail patterns in migrating cells. These observations confirm the theoretical predictions of stress concentration zones and the role of branch density in directing propulsion. Moreover, the chapter distinguishes between spontaneous symmetry breaking and cue‑induced breaking, showing that external signals (e.g., membrane receptor activation) or pre‑existing structural asymmetries can bias the initial conditions and fix the direction of motion.

Finally, the authors explore practical implications of manipulating material properties and growth dynamics. Chemical agents that stiffen the actin gel (e.g., actin‑binding drugs) increase the effective elastic modulus, dampening propulsion and limiting directional changes. Conversely, inhibitors of capping proteins or cofilin alter polymerization rates, delaying symmetry breaking but potentially causing abrupt “switch‑like” transitions under certain conditions. These insights open avenues for antimicrobial strategies that disrupt pathogen motility and for engineering artificial cells or microrobots whose movement can be programmed by tuning actin network mechanics and kinetics. The chapter concludes that a multiscale, integrative approach is essential for unraveling actin‑based motility and for harnessing its principles in both biomedical and bio‑inspired engineering applications.