Reconstitution of Listeria motility: implications for the mechanism of force transduction.

Listeria monocytogenes and some other infectious bacteria polymerize their host cell's actin into tails that propel the bacteria through the cytoplasm. Here we show that reconstitution of this behavior in simpler media resolves two aspects of the mechanism of force transduction. First, since dilute reconstitution media have no cytoskeleton, we consider what keeps the tail from being pushed backward rather than the bacterium being propelled forward. The dependence of the partitioning of motion on the friction coefficient of the tail is derived. Consistent with experiments, we find that the resistance of the tail to motion is sensitive to its length. That even small tails are stationary in intact cells is attributed to anchoring to the cytoskeleton. Second, the comparatively low viscosity of some reconstitution media magnifies the effects of diffusion, such that a large gap will develop between the bacterium and its tail if they are unattached. At the viscosities of diluted platelet extracts, steady-state gaps of several bacterium lengths are predicted. Since such gaps are not observed, we conclude that Listeria must be attached to their tails. We consider what purposes such attachments might serve under physiological conditions. The implications for related pathogens and amoeboid locomotion are also discussed.