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Defining a Core Set of Actin Cytoskeletal Proteins Critical For View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Cell Host & Microbe Article Defining a Core Set of Actin Cytoskeletal Proteins Critical for Actin-Based Motility of Rickettsia Alisa W. Serio,1 Robert L. Jeng,1,3 Cat M. Haglund,1 Shawna C. Reed,2 and Matthew D. Welch1,* 1Department of Molecular and Cell Biology 2Microbiology Graduate Group University of California, Berkeley, Berkeley, CA 94720, USA 3Present address: Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA *Correspondence: [email protected] DOI 10.1016/j.chom.2010.04.008 SUMMARY monocytogenes, Shigella flexneri, Mycobacterium marinum, and Burkholderia pseudomallei (Gouin et al., 2005). Many Rickettsia species are intracellular bacterial Interestingly, the filament architecture in SFG Rickettsia actin pathogens that use actin-based motility for spread tails differs substantially from that of other pathogens. Actin fila- during infection. However, while other bacteria ments in Rickettsia tails are long and organized into parallel assemble actin tails consisting of branched bundles, similar to actin in cellular protrusions such as filopodia networks, Rickettsia assemble long parallel actin and microvilli (Gouin et al., 1999; Van Kirk et al., 2000). In bundles, suggesting the use of a distinct mechanism contrast, L. monocytogenes tails are composed of a sheath of longer bundled filaments surrounding a core of shorter filaments for exploiting actin. To identify the underlying mech- organized in Y-branched arrays (Brieher et al., 2004; Cameron anisms and host factors involved in Rickettsia parkeri et al., 2001; Sechi et al., 1997), similar to actin in lamellipodia actin-based motility, we performed an RNAi screen (Svitkina and Borisy, 1999). These differences in actin organiza- targeting 115 actin cytoskeletal genes in Drosophila tion presumably reflect differences in how actin filaments are cells. The screen delineated a set of four core assembled and organized at the bacterial surface. proteins—profilin, fimbrin/T-plastin, capping protein, Well-studied pathogens such as L. monocytogenes and S. and cofilin—as crucial for determining actin tail flexneri assemble and organize actin by recruiting and activating length, organizing filament architecture, and the host Arp2/3 complex, an actin-nucleating factor that poly- enabling motility. In mammalian cells, these proteins merizes Y-branched filament networks and is localized to bacte- were localized throughout R. parkeri tails, consistent rial actin tails (Gouin et al., 2005). Both pathogens activate the with a role in motility. Profilin and fimbrin/T-plastin Arp2/3 complex by expressing surface proteins that either mimic or recruit host nucleation-promoting factors (NPFs) (Boujemaa- were critical for the motility of R. parkeri but not Paterski et al., 2001; Egile et al., 1999; Skoble et al., 2001; Suzuki Listeria monocytogenes. Our results highlight key et al., 1998). L. monocytogenes and S. flexneri motility can be re- distinctions between the evolutionary strategies constituted in vitro in a mix of purified proteins including actin, and molecular mechanisms employed by bacterial Arp2/3 complex, capping protein, and actin depolymerizing pathogens to assemble and organize actin. factor (ADF/cofilin) (Loisel et al., 1999). Thus, a small set of core proteins that control actin dynamics and organization is sufficient to drive motility. INTRODUCTION In contrast, for Rickettsia, the molecular mechanism of actin assembly and organization is not well understood. The Rickettsia are Gram-negative, obligate-intracellular bacteria that R. rickettsii sca2 gene was recently reported to be required for are transmitted to mammals by blood-feeding arthropod motility and virulence, but the mechanism was not investigated vectors, and many species cause diseases such as spotted fever (Kleba et al., 2010). In addition, most SFG Rickettsia genomes and typhus (Walker and Ismail, 2008). During infection in encode an NPF for the Arp2/3 complex called RickA, which mammals, Rickettsia induce phagocytosis by endothelial cells can direct Arp2/3 complex-dependent motility of plastic beads and then rapidly escape from the phagosome into the cytosol, in cell extracts, but RickA expression is not directly correlated where they replicate. Once in the cytosol, most spotted fever with Rickettsia spp. pathogenicity (Gouin et al., 2004; Jeng group (SFG) Rickettsia species, as well as the typhus group et al., 2004; Ogata et al., 2001). There is also conflicting evidence (TG) species R. typhi, assemble actin tails at their surface and as to whether the Arp2/3 complex is (Gouin et al., 2004) or is not undergo actin-based motility (Heinzen et al., 1993; Teysseire (Gouin et al., 1999; Van Kirk et al., 2000) associated with motile et al., 1992). Rickettsia are then propelled throughout the cell Rickettsia, and whether the complex is (Gouin et al., 2004)oris and into protrusions, mediating cell-to-cell spread and not (Balraj et al., 2008; Harlander et al., 2003; Heinzen, 2003) enhancing virulence (Kleba et al., 2010). The ability to hijack functionally important for bacterial motility. Numerous other the actin cytoskeleton to drive movement is shared between actin-binding proteins have been localized to Rickettsia tails Rickettsia and other bacterial pathogens including Listeria including profilin, VASP, a-actinin, and filamin (Gouin et al., 388 Cell Host & Microbe 7, 388–398, May 20, 2010 ª2010 Elsevier Inc. Cell Host & Microbe Host Proteins Critical for Rickettsia Motility 1999; Van Kirk et al., 2000). However, their function in Rickettsia adapters and membrane-cytoskeleton linkers; (5) myosin motility has not yet been investigated, and the actin cytoskeletal motors; and (6) cytoskeletal signaling proteins. proteins required for Rickettsia motility have yet to be defined. Of the 18 genes implicated in infection, RNAi targeting of eight Based on the unique filament architecture in Rickettsia actin resulted in a decrease in bacteria per cell, including those encod- tails, we hypothesized that a distinct set of host cytoskeletal ing the Arp2/3 complex subunit Arp2, the NPFs SCAR and proteins is critical for Rickettsia motility compared to other path- WASP, the SH2/SH3 adaptor protein Drk, the GTPase Mtl, the ogens. To identify the host factors that are required for Rickettsia motors myosin V and myosin VI, and the actin-associated motility, we employed RNA interference (RNAi) to examine the protein Dah. These proteins might enhance R. parkeri infection function of over 100 actin cytoskeletal proteins in Drosophila by promoting internalization, motility or spread. RNAi of ten melanogaster cells. We identified numerous proteins that play others resulted in an increase in bacteria per cell, which was roles in Rickettsia infection and actin-based motility. In partic- caused by an increase in cell size in some cases (allowing ular, profilin, fimbrin/T-plastin, capping protein, and ADF/cofilin more bacteria to accumulate in a single cell), or could also reflect were essential for actin tail morphology and motility. In mamma- more efficient bacterial internalization, replication, motility, lian cells, profilin and fimbrin/T-plastin were specifically impor- and/or spread. tant for motility of R. parkeri but not for L. monocytogenes. The screen also identified 20 genes implicated in actin-based Thus, our results identify a distinct set of core host proteins motility. These included genes encoding Arp2/3 complex that play a role in Rickettsia actin-based motility. subunits (ARPC3, ARPC4, and ARPC5), the G-actin-binding proteins profilin and cyclase-associated protein (CAP), the severing/depolymerizing protein cofilin, the cofilin phosphatase RESULTS slingshot, the actin bundling proteins fimbrin and a-actinin, the GTPases Rac1 and Rac2, the kinase ROCK, the motors myosin RNAi Screening Identifies Proteins Important IA and II, and the endocytic protein Hip1R. Five of the 20 genes— for R. parkeri Infection and Actin Tail Formation encoding SCAR, Dah, Drk, Mtl, and myosin VI—were also impli- Because of the amenability of Drosophila S2R+ cells to RNAi- cated in infection, suggesting that defects in tail formation and mediated gene silencing and the natural ability of Rickettsia to infection can result from inhibition of common pathways. Thus, infect arthropod cells, we used these cells for RNAi screening the RNAi screen identified numerous candidate proteins that to identify host proteins that play a role in Rickettsia actin-based might perform important functions in actin-based motility. motility. We found that R. parkeri, a member of the SFG that causes mild human disease (Paddock et al., 2008), readily RNAi of Numerous Targets Causes Defects in Actin Tail invaded and replicated in S2R+ cells. Moreover, R. parkeri Length and Morphology motility occurred at similar rates in S2R+ (13.0 ± 0.3 mm/min, To identify those target genes that function specifically in actin- n = 23) and mammalian COS7 (13.8 ± 0.43 mm/min, n = 26) cells, based motility, we sought a phenotypic parameter more directly resulting in the formation of actin tails with similar morphology in linked to this process. Previous work with L. monocytogenes both cell types (see Figure S1A available online). This suggests showed that the length of actin tails associated with moving that the mechanism of motility is conserved between species. bacteria directly correlates with the rate of movement (Theriot We conducted an RNAi screen by targeting 115 actin cyto- et al., 1992). We therefore targeted the 34 genes identified in skeletal genes and two noncytoskeletal control genes the original screen using RNAi and measured the effect on actin (Table S1). The list of targets was expanded from a previous tail length. RNAi of 20 genes resulted in significantly shorter actin screen that assessed the role of cytoskeletal proteins in lamellae tails than those in untreated control cells, with the most dramatic formation (Rogers et al., 2003). Cells were treated with dsRNA for reductions (>66%) observed after targeting profilin, fimbrin, and 4 days, infected with R. parkeri for 2 days, and then bacteria and capping protein (Figure 1A).
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