Effect of hfq-deletion on Salmonella transcriptome
Ontology highlight
ABSTRACT:
ORGANISM(S): Salmonella enterica
PROVIDER: GSE8985 | GEO | 2008/08/23
SECONDARY ACCESSION(S): PRJNA102449
REPOSITORIES: GEO
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Project description:The expression profile of an S. Typhimurium hfq mutant-strain was compared to the parental strain under 2 different growth conditions; early stationary phase and SPI-1 (Salmonella pathogenicity island 1) inducing condition. Keywords: Genetic modification This study comprises two separate experiments performed under different growth conditions, were the gene expression profile was compared to that of the parental strain. Three biological replicates were performed for each strain and condition. For this study, we used Salmonella genomic DNA as the comparator which also acted as the control for spot quality.
2008-08-23 | E-GEOD-8985 | biostudies-arrayexpress
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.
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Project description:Salmonella enterica serovar Typhimurium is known to synthesize and respond to the cell signaling molecule, autoinducer-2 (AI-2). The luxS gene is involved in the synthesis of AI-2. We have previously shown that luxS controls a variety of bacterial processes in S. Typhimurium. In this study we identified the genes regulated by AI-2 in the Cell-Free supernatant of S. Typhimurium using mRNA samples from isogenic luxS gene mutant of S. Typhimurium strain 87-26254 grown in LB media in the presence of S. Typhimurium wild type CFS / absence AI-2 (mutant CFS of S. Typhimurium). In the presence of AI-2 in CFS, 758 genes were significantly regulated. Interstingly, AI-2 in CFS caused the down-regulation of 39 genes in Salmonella Pathogenicity Island-1 (SPI-1).
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Project description:<p><em>Salmonella Typhimurium</em> establishes systemic infection by replicating in host macrophages. Here we show that macrophages infected with <em>S. Typhimurium</em> exhibit upregulated glycolysis and decreased serine synthesis, leading to accumulation of glycolytic intermediates. The effects on serine synthesis are mediated by bacterial protein SopE2, a type III secretion system (T3SS) effector encoded in pathogenicity island SPI-1. The changes in host metabolism promote intracellular replication of <em>S. Typhimurium</em> via two mechanisms: decreased glucose levels lead to upregulated bacterial uptake of 2- and 3-phosphoglycerate and phosphoenolpyruvate (carbon sources), while increased pyruvate and lactate levels induce upregulation of another pathogenicity island, SPI-2, known to encode virulence factors. Pharmacological or genetic inhibition of host glycolysis, activation of host serine synthesis, or deletion of either the bacterial transport or signal sensor systems for those host glycolytic intermediates impairs <em>S. Typhimurium</em> replication or virulence.</p>
2024-05-22 | MTBLS2347 | MetaboLights
Project description:Salmonella enterica serovar Typhimurium is known to synthesize and respond to the cell signaling molecule, autoinducer-2 (AI-2). The luxS gene is involved in the synthesis of AI-2. We have previously shown that luxS controls a variety of bacterial processes in S. Typhimurium. In this study we identified the genes regulated by AI-2 using mRNA samples from isogenic luxS gene mutant of S. Typhimurium strain 87-26254 grown in LB media in the presence/absence of in vitro synthesized AI-2. In the presence of in vitro synthesized AI-2, 536 genes were significantly (p<0.05) regulated. Interestingly, in vitro synthesized AI-2 caused the down-regulation of 39 genes in Salmonella Pathogenicity Island-1 (SPI-1) including the transcriptional regulators hilA, hilD, and invF.
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Project description:LeuO, initially identified as a leucine regulator in Escherichia coli, has since been identified as a global regulator required for bacterial pathogenicity in a broad range of bacteria, including gram-negative pathogens, such as Salmonella, Shigella, and Vibrio; and gram-positive bacteria, such as Streptococcus pneumoniae. However, the regulatory roles and targets of LeuO vary among species. In the Salmonella enterica subsp. enterica serovar Typhimurium (S. Typhimurium), LeuO represses the transcription of Salmonella pathogenicity island (SPI)-1, thus diminishing the ability of the bacteria to invade host cells. However, its regulatory effect on SPI-2, essential for survival within macrophages, remains poorly understood. This study aimed to determine the regulatory role of LeuO in the intracellular persistence of S. Typhimurium. Overexpression of LeuO repressed the transcription of SPI-2 genes and accordingly decreased its protein levels. Chromatin immunoprecipitation sequencing revealed the genome-wide binding sites of LeuO in S. Typhimurium 14028 and identified a distinctive 23-nucleotide motif with high similarity to that previously discovered in E. coli. Notably, multiple LeuO-binding sites were predicted within SPI-2, primarily adjacent to the ssrA and ssrB loci. In vitro binding assays verified the high binding affinity between LeuO and three specific motifs located at positions -35 to -12 (ssrA1),+231 to +254 (ssrA2) near ssrA, and at positions -622 to -599 (ssrB3) near ssrB, relative to their transcription start sites. Furthermore, LeuO overexpression abolished the transcription of lacZ fused to the ssrA promoter containing ssrA1 and ssrA2, suggesting the direct repression of ssrA via LeuO-binding. The absence of LeuO increased the intracellular survival of S. Typhimurium within macrophages, whereas its overexpression attenuated bacterial persistence, which was presumably associated with the downregulation of SPI-2 by LeuO. This study reveals the versatile regulatory mechanisms of LeuO and underscores its pivotal role in modulating SPI-2 expression, thereby providing key insights into the fine tuning of virulence by Salmonella during systemic infection.
2024-11-14 | GSE280231 | GEO
Project description:S. typhimurium 14028 wt, hfq and smpB were harvested from log phase LB (LBlog); (2), stationary phase LB (LBstat); (3) 4h MgM medium pH 5.0 after resuspension of LB stat culture (MgMshock); and (4) log phase MgM medium pH5.0 after 100fold dilution of an LB stat culture (MgMDil). Total RNA was extracted, cDNA labeled and hybridized to a non-redundant Salmonella whole genome PCR product ORF array.
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Project description:Investigation of whole genome gene expression level changes in a Salmonella enterica serovar Typhimurium UK1 delta-iacP mutant, compared to the wild-type strain. IacP is resoponsible for the secretion of virulence effector proteins via the type III secretion system, thereby contributing the virulence of S. Typhimurium. The mutants analyzed in this study are further described in Kim et al. 2011. Role of Salmonella Pathogenicity Island 1 Protein IacP in Salmonella enterica Serovar Typhimurium Pathogenesis. Infection and Immunity 79(4):1440-1450 (PMID 21263021).
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Project description:RNA extracted from representative isolates of each serovar grown to late exponential phase in Luria-Bertani broth showed that transcript abundances of core genes were significantly higher (p < 0.05) than those of accessory genes for all three serovars. Inter-serovar comparisons demonstrated higher transcript abundances for genes related to vitamin B12 biosynthesis, and ethanolamine and 1,2-propanediol utilization in S. Cerro compared to Javiana and Typhimurium, while genes in Salmonella Pathogenicity Island (SPI) 1 had significantly higher transcript abundances in S. Javiana and S. Typhimurium.
2020-05-21 | GSE150943 | GEO
Project description:CorA is the primary Mg2+ channel in Salmonella enterica serovar Typhimurium. A strain lacking corA is attenuated in mice after infection either by oral gavage or intraperitoneal injection. Microarray studies show that several virulence effectors in Salmonella pathogenicity island 1 and Salmonella pathogenicity island 2 are repressed in the corA strain compared to wild type. While these results could be sufficient to explain the virulence deficit, the microarray data suggest additional defects that could also contribute. Motility is significantly reduced in a corA strain whereas enterochelin-dependent iron uptake and curli are upregulated. A corA strain is defective for invasion of and replication within Caco-2 epithelial cells. However, a corA strain does not have a significant survival defect in J774A.1 macrophages. Thus, despite the presence of two other Mg2+ transporters, loss of CorA affects multiple systems which manifests ultimately as a decrease in virulence. Keywords: strain comparison
2008-03-22 | GSE10242 | GEO