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Cell Host Microbe. 2009 Sep 17;6(3):268-78. doi: 10.1016/j.chom.2009.08.006.

Regulatory mimicry in Listeria monocytogenes actin-based motility.

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Section of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT, USA.


The actin-based motility of the intracellular pathogen Listeria monocytogenes relies on ActA, a bacterial factor with a structural domain allowing it to mimic the actin nucleation-promoting activity of host cell proteins of the WASP/WAVE family. Here, we used an RNAi-based genetic approach in combination with computer-assisted image analysis to investigate the role of host factors in L. monocytogenes cell-to-cell spread. We showed that the host cell serine/threonine kinase CK2 is required for efficient actin tail formation by L. monocytogenes. Furthermore, CK2-mediated phosphorylation of ActA regulated its affinity for the actin-nucleating ARP2/3 complex, as is the case for CK2-mediated phosphorylation of WASP and WAVE. Thus, ActA not only displays structural mimicry of WASP/WAVE family members, but also regulatory mimicry, having precisely co-opted the host machinery regulating these proteins. Comparisons based on ActA amino acid sequence suggest that unrelated pathogens that display actin-based motility may have evolved a similar strategy of regulatory mimicry.

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