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Paper 3 Reed et al 2014

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Current Biology 24, 98–103, January 6, 2014 ª2014 Elsevier Ltd All rights reserved http://dx.doi.org/10.1016/j.cub.2013.11.025 Rickettsia Actin-Based Motility Occurs in Distinct Phases Mediated by Different Actin Nucleators Shawna C.O. Reed,1,2,4 Rebecca L. Lamason,1 Viviana I. Risca,3,5 Emma Abernathy,2 and Matthew D. Welch1,2,* 1Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA 2Microbiology Graduate Group, University of California, Berkeley, Berkeley, CA 94720, USA 3Biophysics Graduate Group, University of California, Berkeley, Berkeley, CA 94720, USA Summary Many intracellular bacterial pathogens undergo actin-based motility to promote cell-cell spread during infection [1]. For each pathogen, motility was assumed to be driven by a single actin polymerization pathway. Curiously, spotted fever group Rickettsia differ from other pathogens in possessing two actin-polymerizing proteins. RickA, an activator of the host Arp2/3 complex, was initially proposed to drive motility [2, 3]. Sca2, a mimic of host formins [4, 5], was later shown to be required for motility [6]. Whether and how their activities are coordinated has remained unclear. Here, we show that each protein directs an independent mode of Rickettsia parkeri motility at different times during infection. Early after invasion, motility is slow and meandering, generating short, curved actin tails that are enriched with Arp2/3 complex and cofilin. Early motility re ...
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