Actin‐based motility of intracellular bacteria, and polarized surface distribution of the bacterial effector molecules

Abstract

Several intracellular bacterial pathogens, including species of Listeria, Rickettsia, Shigella, Mycobacteria, and Burkholderia, have evolved mechanisms to exploit the actin polymerization machinery of their hosts to induce actin-based motility, enabling these pathogens to spread between host cells without exposing themselves to the extracellular milieu. Efficient cell-to-cell spread requires directional motility, which the bacteria may achieve by concentrating the effector molecules at one pole of their cell body, thereby restricting polymerization of monomeric actin into actin tails to this pole. The study of the molecular processes involved in the initiation of actin tail formation at the bacterial surface, and subsequent actin-based motility, has provided much insight into the pathogenesis of infections caused by these bacteria and into the cell biology of actin dynamics. Concomitantly, this field of research has provided an opportunity to understand the mechanisms whereby bacteria can achieve a polarized distribution of surface proteins. This review will describe the process of actin-based motility of intracellular bacteria, and the mechanisms by which bacteria can obtain a polarized distribution of their surface proteins.