A Multi-Scale Mechanistic Model for Actin-Propelled Bacteria

Some invasive bacterial pathogens propel themselves intracellularly by hijacking the host cell's actin assembly machinery to polymerize actin. laments into a dense "comet tail'' network of filamentous actin. The bacterium is propelled forward as new actin monomers incorporate into. lament ends positioned at the bacterial surface. How the bacterium remains firmly attached to the elongating end of the actin tail during propulsion remains a central question in actin-based motility. Here, a mechanistic model, based on the. lament end-tracking motor ("actoclampin'') hypothesis, is proposed to explain some emergent features of actin-based propulsion, including the alignment of. laments with the direction of motion, rotation about the axis of motion, and helical trajectories. Simulation of the model shows that these features should arise naturally from diffusion-limited elongation of an ensemble of. laments that are strongly anchored at their elongating ends to the bacterial surface by end-tracking proteins. These results suggest that a persistent torsion and curvature of the actin comet tail does not require a. lament torque (created by insertional elongation of helical. laments), although a small right-handed. lament torque is sufficient to ensure symmetry breaking toward a right-handed torsion.