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NGS genotyping of Francisella tularensis

ABSTRACT: Rapid high resolution genotyping of Francisella tularensis by whole genome sequence comparison of annotated genes.

PROVIDER: PRJEB5252 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR414089_1.fastq.gz	Fastqsanger.gz
	ERR414089_2.fastq.gz	Fastqsanger.gz
	ERR414801.fastq.gz	Fastqsanger.gz
	ERR425052.fastq.gz	Fastqsanger.gz
	ERR431510.fastq.gz	Fastqsanger.gz

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Microarray analysis of human monocytes infected with Francisella tularensis

Project description:Differential expression in human peripheral blood monocytes between F. novicida-infected and uninfected, and between Francisella tularensis tularensis isolate Schu S4 and uninfected. The goal was to examine genomewide transcriptional reponses to these two strains, and identify differentially-regulated genes that may help explain the virulence of Schu S4. Keywords: Immune Response, Human Monocytes, Bacteria, Francisella

2008-08-13 | GSE12108 | GEO

Transcriptome RNA Sequencing Data Sets of Francisella tularensis tularensis SchuS4 upon treatment with various concentrations of Doxycycline or Ciprofloxacin antibiotics

Project description:Francisella tularensis, the etiological agnet of Tularemia is a Category A select agent. Preparedness means for prompt proper antibiotic treatment are of need to prevent morbidity and mortality. While standard antimicrobial susceptibility tests are time consuming, the quantification of the changes in the expression levlels of specific mRNA markers folowing antibiotic exposure may enable a rapid determination of antimicrobial susceptibility. We submit transcriptomic data sets detailing global gene expression of F. tularensis following exposure to Doxycycline or Ciprofloxacin antibiotics.

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An AraC/XylS Family Transcriptional Regulator Modulates the Oxidative Stress Response of Francisella tularensis

Project description:Francisella tularensis is a Gram-negative bacterium that causes a fatal human disease known as tularemia. The Centers for Disease Control have classified F. tularensis as Category A Tier-1 Select Agent. The virulence mechanisms of Francisella are not entirely understood. Francisella possesses very few transcription regulators, and most of these regulate the expression of genes involved in intracellular survival and virulence. The F. tularensis genome sequence analysis reveals an AraC (FTL_0689) transcriptional regulator homologous to the AraC/XylS family of transcriptional regulators. In Gram-negative bacteria, AraC activates genes required for L-arabinose utilization and catabolism. The role of the FTL_0689 regulator in F. tularensis is not known. In this study, we characterized the role of FTL_0689 in gene regulation of F. tularensis and investigated its contribution to intracellular survival and virulence. The results demonstrate that FTL_0689 in Francisella is not required for L-arabinose utilization. Instead, FTL_0689 specifically regulates the expression of the oxidative and global stress response, virulence, metabolism, and other key pathways genes required by Francisella when exposed to oxidative stress. The FTL_0689 mutant is attenuated for intramacrophage growth, and mice infected with the FTL_0689 mutant survive better than wild-type F. tularensis LVS infected mice. Based on the deletion mutant phenotype, FTL_0689 was termed osrR (oxidative stress response regulator). Altogether, this study elucidates the role of the osrR transcriptional regulator in tularemia pathogenesis.

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Lung microenvironment effects on T cells following Francisella tularensis vaccination

Project description:Pulmonary infections often fail to produce long-lived immune memory and the underlying mechanism(s) remain unclear. We undertook a multiomics approach to compare adaptive immunity in two bacterial infections: Bordetella pertussis and Francisella tularensis. Both infections require CD4+ T cells, but B. pertussis results in long-lived memory responses whereas F. tularensis does not. Single cell RNA sequencing and flow cytometry revealed CD4+ T cells favored proliferation immediately after secondary B. pertussis infection but stagnated during F. tularensis challenge. Instead, rapid IFN-γ production by F. tularensis-elicited T cells induced IDO1 expression in endothelial cells, depleting pulmonary tryptophan and increasing kynurenine. This metabolic shift correlated with poor T cell proliferation and retention. Additionally, IDO1 knock-out resulted in larger T cell pools and improved survival during F. tularensis infection. Imaging confirmed the spatial association of immune cell centers and IDO1-expressing macrovascular endothelial cells underscoring the microenvironment’s impact on T cell function. Our study highlights the utility of multiomics in understanding cellular interactions within complex tissues.

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Project description:To understand differences of gene expression profiles between Francisella strains RNA profiles of Francisella strains were generated by deep sequencing, in triplicate, using NovaSeq6000. qRT–PCR validation was performed using SYBR Green assays. Our study represents the first detailed differential transcriptomic analysis of Francisella strains , with biologic replicates, generated by RNA-seq technology.

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Project description:Francisella tularensis Genome sequencing

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