Bacterial spread from cell to cell: beyond actin-based motility

• Intracellular bacteria displaying actin-based motility have evolved specific mechanisms of spread from cell to cell.
• The resolution of Listeria monocytogenes protrusions relies on the dynamics of the actin cytoskeleton.
• The resolution of Shigella flexneri protrusions relies on the type III secretion system-dependent manipulation of host-cell tyrosine kinase and phosphoinositide signaling.

Several intracellular pathogens display the ability to propagate within host tissues by displaying actin-based motility in the cytosol of infected cells. As motile bacteria reach cell–cell contacts they form plasma membrane protrusions that project into adjacent cells and resolve into vacuoles from which the pathogen escapes, thereby achieving spread from cell to cell. Seminal studies have defined the bacterial and cellular factors that support actin-based motility. By contrast, the mechanisms supporting the formation of protrusions and their resolution into vacuoles have remained elusive. Here, we review recent advances in the field showing that Listeria monocytogenes and Shigella flexneri have evolved pathogen-specific mechanisms of bacterial spread from cell to cell.