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Gene Expression of F. tularensis LVS in hepatocytic cell line FL83B vs LVS cultured in MH broth

ABSTRACT: Transcriptional profiling of LVS grown in hepatocytic cell line FL83B was compared to that of LVS cultued in MH broth to discover genes important for intracellular growth.

ORGANISM(S): Francisella tularensis subsp. holarctica LVS Francisella tularensis

PROVIDER: GSE43731 | GEO | 2013/01/25

SECONDARY ACCESSION(S): PRJNA187343

REPOSITORIES: GEO

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Gene Expression of F. tularensis LVS in hepatocytic cell line FL83B vs LVS cultured in MH broth

Project description:Transcriptional profiling of LVS grown in hepatocytic cell line FL83B was compared to that of LVS cultued in MH broth to discover genes important for intracellular growth. Two-condition experiment, Intracellular vs. Broth. Biological replicates: 4 Broth, 4 intracellular, independently grown and harvested. One replicate per array.

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Characterization of F. tularensis LVS outer membrane vesicles

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

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