Article

The small RNA chaperone Hfq is required for the virulence of Yersinia pseudotuberculosis

Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Infection and immunity (Impact Factor: 4.16). 03/2010; 78(5):2034-44. DOI: 10.1128/IAI.01046-09
Source: PubMed

ABSTRACT Bacterial small, noncoding RNAs (sRNAs) participate in the posttranscriptional regulation of gene expression, often by affecting protein translation, transcript stability, and/or protein activity. For proper function, many sRNAs rely on the chaperone Hfq, which mediates the interaction of the sRNA with its target mRNA. Recent studies have demonstrated that Hfq contributes to the pathogenesis of a number of bacterial species, suggesting that sRNAs play an essential role in the regulation of virulence. The enteric pathogen Yersinia pseudotuberculosis causes the disease yersiniosis. Here we show that Hfq is required by Y. pseudotuberculosis to cause mortality in an intragastric mouse model of infection, and a strain lacking Hfq is attenuated 1,000-fold compared to the wild type. Hfq is also required for virulence through the intraperitoneal route of infection and for persistence of the bacterium in the Peyer's patches, mesenteric lymph nodes, and spleen, suggesting a role for Hfq in systemic infection. Furthermore, the Deltahfq mutant of Y. pseudotuberculosis is hypermotile and displays increased production of a biosurfactant-like substance, reduced intracellular survival in macrophages, and decreased production of type III secretion effector proteins. Together, these data demonstrate that Hfq plays a critical role in the virulence of Y. pseudotuberculosis by participating in the regulation of multiple steps in the pathogenic process and further highlight the unique role of Hfq in the virulence of individual pathogens.

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    • "OMVs or lysates (20 µg each) were mixed with reducing sample buffer (10% glycerol, 100 mM Tris-HCl, pH 6.8, 2% sodium dodecyl sulfate (SDS), 0.02% bromophenol blue, 5% β-mercaptoethanol) and separated by SDS-PAGE. Proteins were transferred to nitrocellulose membranes for immunblot analyses with antibodies against Pla [74], Ail (Eric Krukonis, University of Detroit Mercy School of Dentistry), Hfq [53], Caf1 (Abcam), and RpoA (Melanie Marketon, Indiana University). "
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    PLoS ONE 09/2014; 9(9):e107002. DOI:10.1371/journal.pone.0107002 · 3.23 Impact Factor
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    • "The spectrum and severity of hfq mutant phenotypes can vary among the different pathogens. For example, Yersinia hfq mutant is hyper-motile [38] but hfq mutation impairs motility in Salmonella, P. aeruginosa and E. coli [8], [13], [30]. Besides, deletion of hfq does prevent RpoS production in Salmonella and E. coli but not in V. cholerae [8], [11]. "
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    • "Also, no flagella were present in an electron micrograph of an E. coli hfq mutant [20]. However, the species-specific role of Hfq in the regulation of motility is illustrated by the increased swarming motility of a Y. pseudotuberculosis hfq mutant as well as increased biosurfactant production [21]. Therefore, it will be interesting to explore further the role of Hfq in the regulation of flagellum production in S39006, and the cause of the decreased motility despite an increase in flagellar gene expression. "
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