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Articles of Significant Interest Selected from This Issue by the Editors

Certain microbial pathogens exploit cellular actin polymerization to disseminate through tissue. Polymerization of actin propels Shigella flexneri to the cell periphery in an N-WASPand Arp2/3-dependent fashion, whereupon the bacteria spread into adjacent cells via plasma membrane protrusions. Heindl et al. (p. 193–203) demonstrate that efficient formation of plasma membrane protrusions by Shigella depends on a distinct cellular pathway of actin polymerization that involves the diaphanous formins. Expression of a dominant interfering construct or knockdown of formin mRNA levels inhibited protrusion formation and bacterial spread. Thus, Shigella usurps two distinct actin polymerization machines during spread.