Abstract
Selection for resistance to the antibiotic fosfomycin (FOS; L-cis 1,2-epoxypropylphosphonic acid, a structural analogue of phosphoenolpyruvate) was used to isolate mutants carrying internal and extended deletions of varying lengths within the ptsHI operon of Salmonella typhimurium. Strains carrying "tight" ptsI point mutations and all mutants in which some or all of the ptsI gene was deleted were FOS resistant. In contrast, strains carrying ptsH point mutations were sensitive to FOS. Resistance to FOS appeared to result indirectly from catabolite repression of an FOS transport system, probably the sn-glycerol-3-phosphate transport system. Resistant ptsI mutants became sensitive to FOS when grown on D-glucose-6-phosphate, which induces an alternate transport system for FOS, or when grown in the presence of cyclic adenosine 3',5'-monophosphate. A detailed fine-structure map of the pts gene region is presented.
MeSH Terms
Anti-Bacterial Agents/pharmacology
Biological Transport, Active
Chromosome Mapping
Chromosomes, Bacterial
Cyclic AMP/pharmacology
Drug Resistance, Microbial
Fosfomycin/metabolism,pharmacology
Mutation
Operon
Phosphotransferases/biosynthesis
Salmonella typhimurium/drug effects,enzymology
Chemicals
Anti-Bacterial Agents
Fosfomycin
Cyclic AMP
Phosphotransferases
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Cordaro J C
Melton T
Stratis J P
Atagün M
Gladding C
Hartman P E
Roseman S
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