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. 2011 Oct 3;195(1):7–17. doi: 10.1083/jcb.201103148

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© 2011 Haglund and Welch

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 4. — Exit strategies of diverse intracellular pathogens use actin. Chlamydia (yellow) vacuoles are extruded through a cortical constriction, and the plasma membrane seals around the constriction point in a manner dependent on actin (red), releasing a double-membrane–bound bacterial compartment. The extrusion pathway appears to require myosin II and N-WASP for initiation and Rho for detachment of the extruded vacuole from the host cell. Listeria and Shigella (green), propelled by actin-based motility, enter plasma membrane protrusions and are taken up by neighboring cells. Cadherins, ezrin, mDia, and vinculin have been implicated in protrusion formation. Mycobacterium (purple) exits cells through a plasma membrane break surrounded by a barrel-shaped ejectosome rich in actin, myosin IB, and coronin. In host cells lacking RacH, ejectosomes are not detected and mycobacterial spreading is impaired. Cryptococcus (blue) phagosomes fuse with the plasma membrane, and intermittent actin polymerization around the phagosome, apparently mediated by N-WASP and the Arp2/3 complex, inhibits this fusion.