The sensor kinase QseC regulates the unlinked PmrA response regulator and downstream gene expression in Francisella
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PROVIDER: PRJNA647216 | ENA |
REPOSITORIES: ENA
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Project description:The facultative intracellular bacterial pathogen Francisella tularensis is the causative agent of tularemia in humans and animals. Gram negative bacteria utilize two-component regulatory systems (TCS) to sense and respond to their changing environment. No classical, tandemly arranged sensor kinase and response regulator TCS genes exist in the human virulent Francisella tularensis subsp. tularensis, but orphaned members are present. PmrA is an orphan response regulator responsible for intramacrophage growth and virulence; however, the regulation of PmrA activity is not understood. We and others have shown that PmrA represses the expression of priM, described to encode an anti-virulence determinant. By screening a mutant library for increased priM promoter activity, we identified the sensor kinase homolog QseC as an upstream regulator of priM expression, and this regulation is in part, dependent upon the aspartate phosphorylation site of PmrA (D51). PmrA directly binds to the promoter of priM and a PmrAD51A mutation decreases binding. Several examined environmental signals including epinephrine, which is reported to activate QseC in other bacteria, do not affect priM expression in a manner dependent on PmrA. Intramacrophage survival assays also question the finding that PriM is an anti-virulence factor. Thus, these data suggest that the PmrA-regulated gene priM is regulated by an uncoupled TCS QseC-PmrA (QseB) in Francisella.
2020-07-20 | GSE154698 | GEO
Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell M-bM-^@M-^S to M-bM-^@M-^S cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes. Comparison of transcriptional regulation of enteropathogenic E. coli serotype O55:H7 wild type and the qseC mutant in the absence or presence of epinephrine signal to identify the regulated targets
2013-01-08 | E-GEOD-43325 | biostudies-arrayexpress
Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell – to – cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes.
2013-01-08 | GSE43325 | GEO
Project description: Not available
| S-EPMC7549357 | biostudies-literature
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.
2022-05-31 | GSE174793 | GEO
Project description:ReeS, previously named as CPE1512, was originally annotated as the only hybrid sensor histidine kinase/response regulator in Clostridium perfringens. Further evidence suggests that ReeS is more likely to function as an orphan sensor histidine kinase. A reeS deletion mutant was constructed and the transcriptome analysed using microarrays.
2013-08-31 | GSE36786 | GEO
Project description:“Stress, survival and virulence: the multi-faceted host/microbial interactions.” Bacteria employ epinephrine and norepinephrine, which converge to distinct bacterial crucial processes, like survival and pathogenicity. A novel stress periplasmic membrane protein belonging to previously described BOF family, protein renamed here SrpP, and together with membrane sensor kinase QseC has an essential role in stress response and virulence of S. Typhimurium. SrpP employs its predicted binding pocket, specifically the SrpPE110 residue, and interacts with lipid A modification enzyme, LpxO dioxygenase. Upon this interaction SrpP in S. Typhimurium finely manages multiple membrane functions to culminate in survival upon stress and pathogenesis in vivo, connecting host-stress chemical signaling to cell stress in bacteria. Comparison of sensor histidine kinase qseC mutant expression levels versus wild type strain.
2012-05-31 | E-GEOD-38353 | 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:In this experiment the transcriptional profile of the Pseudomonas aeruginosa PA14 two-component sensor kinase PA4398 was investigated under swarming conditions using DNA microarrays. To this aim three independent cultures of the PA14 wild-type and the PA4398 mutant were grown until mid-log phase in Luria-Bertani broth following an incubation on BM2-swarm plates containing 0.1 % (wt/vol) casaminoacids and 0.5 % (wt/vol) agar for 20 h at 37 °C. Subsequent total RNA was extracted from the leading edge of dendritic swarm colonies and analyzed by microarrays.
2015-01-02 | E-MTAB-2540 | biostudies-arrayexpress
Project description:Comparison of expression profiles of strains of Francisella to identify virulence factors We used custom microarrays to detail the global gene expression of four strains of Francisella (Schu4, LVS, OR960246, U112) and identified distinct classes of differentially expressed genes during this process.
2015-05-02 | GSE68478 | GEO