Project description:Here, we adapted and improved our FASTBAC-Seq method originally designed in Helicobacter pylori to investigate T1TAs in the model organism Escherichia coli. Our approach combines a life and death selection with deep-sequencing to assess the killing capability of a toxin and obtain an overview of single-nucleotide substitutions suppressing the toxin expression or activity in absence of its antitoxin. As a proof of concept, we revisited the regulation of the plasmidic hok/Sok T1TA system.
Project description:The purpose of the present study was to elucidate in more details the molecular mechanisms of neutrophil-mediated inflammation. We therefore investigated the time-dependent stimulatory potential of LPS from Escherichia coli on cytokine response in neutrophil-like HL-60 cells. <br><br>To get a general overview on the total mRNA changes in DMSO-differentiated HL-60 cells, we performed whole-transcript analysis of LPS-stimulated dHL-60 cells after 2h and 6h of LPS treatment. The samples were collected from three independent experiments from three different passages in cell culture. Non-stimulated dHL-60 cells served as control. We identified the differentially expressed cytokine genes implicated in the human inflammatory response and prominent for their role in neutrophil-mediated inflammatory processes.
