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- W1792186902 abstract "Recalcitrance of genetically susceptible bacteria to antibiotic killing is a hallmark of bacterial drug tolerance. This phenomenon is prevalent in biofilms, persisters, and also planktonic cells and is associated with chronic or relapsing infections with pathogens such as Staphylococcus aureus. Here we report the in vitro evolution of an S. aureus strain that exhibits a high degree of nonsusceptibility to daptomycin as a result of cyclic challenges with bactericidal concentrations of the drug. This phenotype was attributed to stationary growth phase-dependent drug tolerance and was clearly distinguished from resistance. The underlying genetic basis was revealed to be an adaptive point mutation in the putative inorganic phosphate (Pi) transporter gene pitA. Drug tolerance caused by this allele, termed pitA6, was abrogated when the upstream gene pitR was inactivated. Enhanced tolerance toward daptomycin, as well as the acyldepsipeptide antibiotic ADEP4 and various combinations of other drugs, was accompanied by elevated intracellular concentrations of Pi and polyphosphate, which may reversibly interfere with critical cellular functions. The evolved strain displayed increased rates of survival within human endothelial cells, demonstrating the correlation of intracellular persistence and drug tolerance. These findings will be useful for further investigations of S. aureus drug tolerance, toward the development of additional antipersister compounds and strategies." @default.
- W1792186902 created "2016-06-24" @default.
- W1792186902 creator A5007885643 @default.
- W1792186902 creator A5036585309 @default.
- W1792186902 creator A5041629489 @default.
- W1792186902 creator A5042002786 @default.
- W1792186902 creator A5061586847 @default.
- W1792186902 creator A5072657067 @default.
- W1792186902 date "2015-09-01" @default.
- W1792186902 modified "2023-10-13" @default.
- W1792186902 title "A Novel Point Mutation Promotes Growth Phase-Dependent Daptomycin Tolerance in Staphylococcus aureus" @default.
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- W1792186902 doi "https://doi.org/10.1128/aac.00643-15" @default.
- W1792186902 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4538524" @default.
- W1792186902 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26100694" @default.
- W1792186902 hasPublicationYear "2015" @default.