title: A mutation in the poxA gene of Salmonella enterica serovar Typhimurium alters protein production, elevates susceptibility to environmental challenges, and decreases swine colonization.
abstract: Control of foodborne Salmonella within the farm-retail continuum is a complex issue since over 2500 serovars of Salmonella exist, the host range of Salmonella spp. varies greatly, and Salmonella is environmentally ubiquitous. To identify Salmonella enterica serovar Typhimurium (Salmonella Typhimurium) genes important for pathogen survival, our research group previously screened a signature-tagged mutagenesis bank in an ex vivo swine stomach content assay. A mutation in the poxA gene, a member of the gene family encoding class-II aminoacyl-tRNA synthetases, decreased survival of Salmonella Typhimurium in the ex vivo swine stomach content assay. In the current study, complementation with a plasmid-encoded poxA gene restored survival of the poxA mutant to the level of the parental, wild-type strain. In vivo analysis of the poxA mutant in the natural porcine host revealed significantly reduced fecal shedding of Salmonella, decreased colonization of the tonsils, and decreased detection of the mutant strain in the cecal contents of the pigs at 7 days postinoculation (p < 0.05). Body temperature (fever) of the pigs inoculated with wild-type Salmonella Typhimurium was significantly higher than that of pigs inoculated with the poxA mutant (p < 0.05). Two-dimensional gel electrophoresis revealed characteristic differences in the protein profile of the poxA mutant relative to the wild-type strain, indicating that deletion of poxA in Salmonella Typhimurium exerts selective effects on translation and/or posttranslational modifications of mRNA species that are necessary for stress survival and colonization of the natural swine host.
authors.affiliation: Food Safety and Enteric Pathogens Research Unit, National Animal Disease Center, Agricultural Research Service, U.S. Department of Agriculture, 1920 Dayton Ave., Room 1403, Ames, IA 50010, USA. shawn.bearson@ars.usda.gov
authors.forename: Shawn M D
authors.initials: SM
authors.lastname: Bearson
authors.forename: Bradley L
authors.initials: BL
authors.lastname: Bearson
authors.forename: Brian W
authors.initials: BW
authors.lastname: Brunelle
authors.forename: Vijay K
authors.initials: VK
authors.lastname: Sharma
authors.forename: In Soo
authors.initials: IS
authors.lastname: Lee
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000096:biosynthesis / Q000737:chemistry / Q000235:genetics / Q000502:physiology; D057138:Bacterial Shedding; D018988:Bacterial Translocation; D002432:Cecum / Q000382:microbiology; D002460:Cell Line; D005243:Feces / Q000382:microbiology; D005260:Female; D005334:Fever / Q000209:etiology; D005767:Gastrointestinal Diseases / Q000382:microbiology / Q000503:physiopathology / Q000662:veterinary; D005798:Genes, Bacterial; D006801:Humans; D008250:Lysine-tRNA Ligase / Q000235:genetics / Q000502:physiology*; D008297:Male; D050296:Microbial Viability; D009154:Mutation; D014066:Palatine Tonsil / Q000382:microbiology; D014176:Protein Biosynthesis; D012481:Salmonella Infections, Animal / Q000382:microbiology* / Q000503:physiopathology; D012486:Salmonella typhimurium / Q000201:enzymology / Q000235:genetics* / Q000472:pathogenicity* / Q000502:physiology; D034421:Sus scrofa
chemical_list: D001426:Bacterial Proteins; D008250:Lysine-tRNA Ligase