Project description:In order to identify genes that were differentally regulated upon oral infection with EPEC, we isolated 8 days post-infection intestinal epithelial cells (IECs) from the small intestine of C57BL/6 neonate mice that were left untreated or orally infected with 5x104 WT EPEC E2348/69 or with 5x104 of the isogenic mutant ΔescV on their first day of life.
Project description:Compared the transcriptome of wild type EPEC with that of an isogenic Δhfq mutant. Comparing activating- conditions:growth on DMEM at 37°C to mid exponential growth phase (e.g., OD600=0.3). In these conditions EPEC strongly expresses its major virulence components, T3SS and BFP, mimicking infection. Non-activating conditions: overnight growth of static culture on LB medium at 37°C where virulence factors are not expressed.
Project description:RIL-seq experiment of EPEC hfq-flag mutant, in activating- conditions:growth on DMEM at 37°C to mid exponential growth phase (e.g., OD600=0.3). In these conditions EPEC strongly expresses its major virulence components, T3SS and BFP, mimicking infection. Non-activating conditions: overnight growth of static culture on LB medium at 37°C where virulence factors are not expressed. RIL-seq experiments are designed to reveal the interactions of sRNA and their targets.
Project description:Global transcriptional analysis of the EPEC prototype strain E2348/69 and its plasmid mutants containing a deletion of perABC, or missing the entire EAF plasmid (strain JPN15).
Project description:To gain mechanistic insights into this phenomenon, we characterized the regulatory role of Rnr in the virulence of prototype EPEC strain E2348-69 by genetic, biochemical, and human organoid-based approaches. Accordingly, RNA-seq analysis revealed more than 500 genes differentially regulated by Rnr, including the type-3 secretion system (T3SS).
