Project description:PacBio SMRT-seq of wild-type, ∆metJ, and ∆dam Salmonella enterica serovar Typhimurium grown under SPI-1-inducing and SPI-2-inducing conditions.
Project description:An RNA-seq analysis of wild-type Salmonella enterica serovar Typhimurium and ∆metJ isogenic mutant grown under SPI-1-inducing and SPI-2-inducing conditions.
Project description:An RNA-seq analysis of wild-type Salmonella enterica serovar Typhimurium and ∆ydhJ isogenic mutant grown under SPI-1-inducing and SPI-2-inducing conditions.
Project description:Mucus forms a critical barrier against enteric pathogens like Salmonella enterica serovar Typhimurium. While in vivo studies indicate that secreted, gel-forming mucins and specifically Core 3 glycosylation are protective against S. Typhimurium, the molecular mechanisms involved remain unclear. Here, we measure gene expression changes in Salmonella enterica serovar Typhimurium LT2 following growth in SPI-1 inducing medium (LB + 0.3M NaCl) with or without purified MUC2 (0.1%, w/v), MUC2 glycans (0.1%, w/v), a pool of monosaccharide components comprised of D-galactose, D-GalNAc, D-GlcNAc, D-fuc, and Neu5Ac (0.1%, w/v), or specific individual mucin sugars, namely N-acetyl galactosamine (GalNAc) (0.2%, w/v) and N-acetyl glucosamine (GlcNAc) (0.2%, w/v). Notably, we find MUC2, MUC2 glycans, and to a lesser extent,D-GalNAc and D-GlcNAc downregulate SPI-1 gene expression.
Project description:HilD is a regulator of Salmonella pathogenicity island 1 (SPI-1) virulence genes in Salmonella enterica serovar Typhimurium. To identify novel HilD-regulated genes, we mapped the genome-wide association of HilD in S. Typhimurium under SPI-1-inducing conditions (high salt, low aeration) using ChIP-seq. HilD was C-terminally tagged with 3 FLAG tags in strain 14028s.
Project description:We report the changes in transcriptional landscape that occur under anaerobic conditions in the absence of a DMSO reductase in Salmonella enterica subsp. enterica serovar Typhimurium strain 14028s. By comparing the transcriptome of the parental, wild-type Salmonella to the transcriptome of a ∆dmsABC strain, we identified that there was a significant upregulation of SPI-2 genes in the ∆dmsABC strain.
Project description:Bacterial genotoxins, produced by several Gram-negative bacteria, induce DNA damage in the target cells. While the responses induced in the host cells have been extensively studied in vitro, the role of the genotoxins as effectors during the course of acute and chronic infections remains poorly characterized.To address this issue, we assessed the effects of the Salmonella enterica genotoxin, known as typhoid toxin, in in vivo models of murine chronic infections. Immunocompetent mice were chronically infected with isogenic S. enterica, serovar Typhimurium (S. Typhimurium) strains, encoding either a functional (MC71-TT) or an inactive (MC71-DcdtB) typhoid toxin. Keywords: salmonella typhimurium, bacterial genotoxins, typhoid toxin, chronic infection, mice model
Project description:To cause disease, Salmonella enterica serovar Typhimurium requires two type-III secretion systems, encoded on Salmonella Pathogenicity Islands 1 and 2 (SPI-1 and -2). These secretion systems serve to deliver virulence proteins, termed effectors, into the host cell cytosol. While the importance of these effector proteins to promote colonization and replication within the host has been established, the specific roles of individual secreted effectors in the disease process are not well understood. In this study, we used an in vivo gallbladder epithelial cell infection model to study the function of the SPI-2-encoded effector, SseL. Deletion of the sseL gene resulted in bacterial filamentation and elongation and unusual localization of Salmonella within infected epithelial cells. Infection with the ΔsseL strain also caused dramatic changes in lipid metabolism and led to massive accumulation of lipid droplets in infected cells. Some of these changes were investigated through metabolomics of gallbladder tissue. This phenotype was directly attributed to the deubiquitinase activity of SseL, as a Salmonella strain carrying a single point mutation in the catalytic cysteine resulted in the same phenotype as the deletion mutant. Excessive buildup of lipids due to the absence of a functional sseL gene was also observed in S. Typhimurium-infected livers. These results demonstrate that SseL alters host lipid metabolism in infected epithelial cells by modifying ubiquitination patterns of cellular targets.
