GSE135009
Genome-wide screening of VxrB binding sites in Vibrio cholerae
Bactericidal antibiotics are powerful drugs because they not only inhibit essential bacterial functions, but convert them into toxic processes. Many bacteria are remarkably tolerant against antibiotics, due to inducible damage repair responses. How these responses promote whole population tolerance in important human pathogens is poorly understood. The two-component system VxrAB of the diarrheal pathogen Vibrio cholerae, a model system for tolerance against cell wall damaging (e.g., beta-lactam) antibiotics, is required for high-level beta-lactam tolerance. Here, we report the mechanism of VxrAB-mediated survival. We find that ?-lactam antibiotics inappropriately induce the Fur-regulated iron starvation response, causing an increase in intracellular free iron and colateral oxidative damage. VxrAB reduces antibiotic-induced toxic influx of Fe by downregulating iron importers and induces cell wall synthesis functions to counteract cell wall damage. Our results highlight the complex responses elicited by antibiotics and suggest that the ability to counteract diverse stresses promotes high-level antibiotic tolerance. Overall design: To identify VxrB direct target genes in Vibrio cholerae genome, we sequenced the DNA samples which were pull downed with 6xHis+VxrB (D78E). Especially, VxrB; two component system sense cell wall damage which is triggered by beta-lactam antibioitc such as penicillin (PenG). So we treated PenG 100 ug/ml in Vibrio cells for 3 hour for full induction of VxrB.To characterize highly reproducible and reliable VxrB direct target genes, we sequenced DNA samples which were pooled with biological six replicates. For the exact control experiment, we also sequenced each input samples and penicillin treated or non treated samples as well.