Genetical studies of serum resistance in Escherichia coli.
One induced and one spontaneous serum-resistant mutant were derived from smooth serum-sensitive Escherichia coli strains. There was little difference in the yield or the O-side-chain-sugar to core-sugar ratio of lipopolysaccharides from the mutants compared with the parental strains. The mutations to serum resistance were not accompanied by increases in either the amount or haemagglutination-inhibiting activity of acidic polysaccharides extracted from the strains. Two colonially rough forms, designated 17fa and 17gb, were isolated from an aged culture of serum-resistant mutant 17. Escherichia coli 17fa appeared to be a som mutant and was rapidly killed by serum. Escherichia coli 17gb retained serological O-specificity, and 17gb lipopolysaccharide contained a full complement of O-side-chains; the strain was killed by serum but only after a delay of 1 h. Escherichia coli K-negative O8 donor Hfr59, which was serum-resistant, was crossed with rough serum-sensitive E. coli strain F470 and his+ recombinants were selected. The majority of his-+ recombinants inherited a full complement of lipopolysaccharide O-side-chains but were killed by serum after a delay of 1 to 2 h. These results suggest that lipopolysaccharide O-side-chains are responsible for a delay in the killing by normal human serum of smooth E. coli strains but that other factors determine full serum resistance. No evidence was found of a role for K-antigens in serum resistance.
D000942:Antigens, Bacterial; D001770:Blood Bactericidal Activity; D002462:Cell Membrane / Q000032:analysis / Q000276:immunology; D003090:Coliphages; D003227:Conjugation, Genetic; D004926:Escherichia coli / Q000276:immunology* / Q000502:physiology; D005796:Genes; D006384:Hemagglutination; D006385:Hemagglutination Inhibition Tests; D008070:Lipopolysaccharides / Q000032:analysis / Q000276:immunology; D009154:Mutation
D000942:Antigens, Bacterial; D008070:Lipopolysaccharides