ColV plasmid-mediated, colicin V-independent iron uptake system of invasive strains of Escherichia coli.
Evidence is presented that ColV plasmid-mediated iron uptake, an important component of the virulence of invasive strains of Escherichia coli, is independent of colicin V synthesis and activity. A mutant of E. coli K-12 deficient in the biosynthesis of enterochelin (strain AN1937) was unable to grow on minimal agar containing the chelating agent alpha,alpha'-dipyridyl unless it was harboring the plasmid ColV-K30 (strain LG1315). Acquisition of the active plasmid-specified iron sequestering system was accompanied by marked enhancement of pathogenicity in experimental infections of mice. Mutants of strain LG1315 were isolated that were defective in iron uptake due to plasmid mutations. They were unchanged with respect to colicin production, but were significantly less virulent than the parent strain. Conversely, mutants isolated as defective in colicin V synthesis were normal for the plasmid-coded iron uptake mechanism and showed the same lethality for infected mice as did strain LG1315. Furthermore, mutations in strain AN1937 which render it resistant or tolerant to the bactericidal action of colicin V did not influence the uptake of iron into plasmid-carrying strains. Cross-feeding tests involving plasmid mutants defective in iron uptake identified two plasmid-specified components of the system, an extracellular iron-chelating compound and a nondiffusible product allowing transport of iron across the bacterial cell membrane.
D000818:Animals; D003086:Bacteriocin Plasmids; D001692:Biological Transport; D002462:Cell Membrane / Q000378:metabolism; D003087:Colicins / Q000235:genetics / Q000378:metabolism*; D004926:Escherichia coli / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity; D007501:Iron / Q000378:metabolism*; D051379:Mice; D009154:Mutation; D010957:Plasmids; D014774:Virulence
D003087:Colicins; D007501:Iron