Ontology highlight
ABSTRACT:
PROVIDER: PRJNA645905 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12211306_1.fastq.gz | Fastqsanger.gz | |||
| SRR12211306_2.fastq.gz | Fastqsanger.gz | |||
| SRR12211307_1.fastq.gz | Fastqsanger.gz | |||
| SRR12211307_2.fastq.gz | Fastqsanger.gz | |||
| SRR12211308_1.fastq.gz | Fastqsanger.gz |
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Project description:Francisella tularensis is a Gram-negative bacterium that is highly virulent in humans, causing the disease tularemia. F. novicida is closely related to F. tularensis and exhibits high virulence in mice, but is avirulent in healthy humans. A F. novicida-specific gene cluster (FTN0451-FTN0456) encodes two proteins with diguanylate cyclase (DGC) and phosphodiesterase (PDE) domains that modulate synthesis and degradation of cyclic di-GMP (cdGMP). No DGC or PDE containing proteins are present in the F. tularensis genome. F. novicida strains lacking either the two DGC/PDE genes cdgA and cdgB or the entire gene cluster (KKF457) are defective for biofilm formation. In addition, expression of CdgB or a heterologous DGC in KKF457 stimulated F. novicida biofilms, even in a strain lacking the biofilm regulator QseB. Genetic evidence suggests that CdgA is predominantly a PDE, while CdgB is predominantly a DGC. The F. novicida qseB strain has reduced cdgA and cdgB transcript levels, demonstrating a F. novicida biofilm signaling cascade that controls cdGMP levels. Interestingly, KKF457 with elevated cdGMP levels exhibited a decrease in intramacrophage replication and virulence in mice, as well as increased growth yield and biofilm formation in vitro. Microarray analyses revealed that cdGMP stimulated the transcription of a chitinase (ChiB) known to contribute to biofilm formation. Our results indicate that elevated cdGMP in F. novicida stimulates biofilm formation and inhibits virulence. We suggest that differences in human virulence between F. novicida and F. tularensis may be due in part to the absence of cdGMP signaling in F. tularensis.
2012-11-30 | GSE39647 | GEO
Project description:Francisella tularensis is a Gram-negative bacterium that is highly virulent in humans, causing the disease tularemia. F. novicida is closely related to F. tularensis and exhibits high virulence in mice, but is avirulent in healthy humans. A F. novicida-specific gene cluster (FTN0451-FTN0456) encodes two proteins with diguanylate cyclase (DGC) and phosphodiesterase (PDE) domains that modulate synthesis and degradation of cyclic di-GMP (cdGMP). No DGC or PDE containing proteins are present in the F. tularensis genome. F. novicida strains lacking either the two DGC/PDE genes cdgA and cdgB or the entire gene cluster (KKF457) are defective for biofilm formation. In addition, expression of CdgB or a heterologous DGC in KKF457 stimulated F. novicida biofilms, even in a strain lacking the biofilm regulator QseB. Genetic evidence suggests that CdgA is predominantly a PDE, while CdgB is predominantly a DGC. The F. novicida qseB strain has reduced cdgA and cdgB transcript levels, demonstrating a F. novicida biofilm signaling cascade that controls cdGMP levels. Interestingly, KKF457 with elevated cdGMP levels exhibited a decrease in intramacrophage replication and virulence in mice, as well as increased growth yield and biofilm formation in vitro. Microarray analyses revealed that cdGMP stimulated the transcription of a chitinase (ChiB) known to contribute to biofilm formation. Our results indicate that elevated cdGMP in F. novicida stimulates biofilm formation and inhibits virulence. We suggest that differences in human virulence between F. novicida and F. tularensis may be due in part to the absence of cdGMP signaling in F. tularensis. A whole genome NibleGen microarray was developed for multiple Francisella subspecies, using shared probes for common genes as well as unique probes for subspecies-specific genes. Included were probes representing the F. novicida U112 genome, with a maximum of 6 probes/gene. RNA was isolated from bacteria and purified as described above. The double-strand cDNA was generated and labeled with Cy3 according to the NimbleGen Gene Expression Array protocol (www.nimblegen.com), using SuperScript Double-Stranded cDNA Synthesis Kit (Invitrogen) and the DNA Labeling Kit (NimbleGen). Microarray results were analyzed using the ArrayStar software (DNASTAR).
2012-11-30 | E-GEOD-39647 | biostudies-arrayexpress
Project description:In many bacteria, the ability to modulate biofilm production relies on specific signaling molecules that are either self-produced or made by neighboring microbes within the ecological niche. We analyzed the potential interspecies signaling effect of the Burkholderia diffusible signal factor (BDSF) on Francisella novicida, a model organism for Francisella tularensis, and demon- strated that BDSF both inhibits the formation and causes the dispersion of Francisella biofilm. Specificity was demonstrated for the cis versus the trans form of BDSF. Using transcriptome sequencing, quantitative reverse transcription-PCR, and activity as- says, we found that BDSF altered the expression of many F. novicida genes, including genes involved in biofilm formation, such as chitinases. Using a chitinase inhibitor, the antibiofilm activity of BDSF was also shown to be chitinase dependent. In addition, BDSF caused an increase in RelA expression and increased levels of (p)ppGpp, leading to decreased biofilm production. These results support our observation that exposure of F. novicida to BDSF causes biofilm dispersal. Furthermore, BDSF upregulated the genes involved in iron acquisition (figABCD), increasing siderophore production. Thus, this study provides the first evidence for a potential role and mechanism of diffusible signal factor (DSF) signaling in the genus Francisella and suggests the possibility of interspecies signaling between Francisella and other bacteria. Overall, this study suggests that in response to the interspecies DSF signal, F. novicida can alter its gene expression and regulate its biofilm formation.
2015-08-19 | GSE72142 | GEO
Project description:Francisella tularensis is a Gram-negative bacteria responsible for tularemia, a disease for which the high prevalence of failure and relapses is a main concern. Directed evolution experiments carried out in presence of antibiotics revealed that acquisition of fluoroquinolones (FQ) resistance was not exclusively related to mutations in DNA gyrase genes which are the first targets of these molecules. Here, using F. tularensis LVS as model, we investigated the role of FupA/B (Fer-Utilization Protein), whose possible contribution to FQ resistance was suggested by genomic analysis of resistant isolates. Using trans-complementation/mutagenesis approaches we definitely connected FupA/B expression to FQ sensitivity. Furthermore, we showed that the virulent strain F. tularensis subsp. tularensis SCHU S4, lacking the homologous FupA protein, exhibited a lower FQ susceptibility. Importantly, the deletion of this lipoprotein promoted an increased secretion of outer membrane vesicles (OMVs). Mass spectrometry-based quantitative proteomic characterization of OMVs from LVS and LVS-∆fupA/B strains led to the identification of 801 proteins among which a subset of 23 proteins exhibited a differential abundance between OMVs from both strains and may therefore contribute to the observed increased FQ susceptibility. We finally demonstrated that OMVs are structural key elements of F. tularensis LVS biofilms providing protection against FQ. Taken together, these results showed that mutations targeting FupA/B contribute to antimicrobial resistance through quantitative and qualitative modulations of OMV biogenesis and biofilm formation, providing new basis for understanding and fighting against Francisella antibiotic resistance and/or persistence.
2019-11-12 | PXD010305 | Pride
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
Project description:These samples are part of an experiment comparing the expression profiles of Francisella tularensis novicida grown in chemically defined medium and bacteria isolated 24 hours post infection of J774 macrophages to identify virulence factors
2017-05-02 | GSE75689 | GEO
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. Experiment Overall Design: Human monocytes were infected with the Schu S4 isolate of Francisella tularensis tularensis (n=4), with F. tularensis subspecies novicida isolate U112 (n=4) or were left uninfected (n=6). Gene expression values were calculated using the gcrma package in R and BioConductor, and limma to identify differentially expressed genes. Submitted here are expression values calculated using R 2.7.1 and BioConductor 2.2 (FreeBSD/amd64) but the original were done using R 2.6.1 and BioConductor 2.1 (FreeBSD/amd64). Twelve other chips were pooled with these 14 for preprocessing.
2008-10-25 | E-GEOD-12108 | biostudies-arrayexpress
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.
2021-10-13 | GSE183001 | GEO
Project description:Prior aerosol exposure to F. tularensis subsp. tularensis, but not the live attenuated strain (LVS) of F. tularensis subsp. holarctica or F. novicida, significantly antagonized the transcriptional response in the lungs of infected mice exposed to aerosolized TLR4 ligand E. coli LPS.
2015-09-30 | GSE65871 | GEO
Project description:Francisella tularensis is a category A select agent based on its infectivity and virulence but disease mechanisms in F. tularensis infection remain poorly understood. A murine pulmonary model of infection was therefore employed to characterize the host immune response to F. tularensis infection and to discern differences in responses to infection with the highly virulent Type A F. tularensis strain Schu4 and to the less virulent Type B live vaccine strain (LVS). Mice were infected intranasally with F. tularensis Schu4 or LVS and organ lesions were assessed 48 and 120 hours after infection. Experiments were also conducted to assess and compare the host immune response to infection using global transcriptional analysis. Mice were infected via low dose aerosol with F. tularensis Schu4 or LVS strains, and transcriptional response in the lungs and spleen was monitored using full mouse genome microarrays at 12, 24, 48, and 120 hours after infection. We found differential and temporal differences in expression of cytokine and chemokine genes, CD molecules, apoptosis, leukocytes and adhesion receptors, and immunological signaling between infection with Schu4 and LVS strains. The transcriptional differences coincided with marked differences in the timing and extent of organ lesions in mice infected with the LVS and Schu4 strains. Thus, these studies revealed both temporal and qualitative differences in the host immune response to infection with virulent F. tularensis Schu4 compared to infection with LVS.
2010-11-01 | GSE22203 | GEO