Abstract
The genetic bases for antibiotic tolerance are obscure. Daptomycin (DAP) is a lipopeptide antibiotic with bactericidal activity against enterococci. Using time-kill assays, we provide evidence for the first time that a deletion of isoleucine in position 177 of LiaF, a member of the three-component regulatory system LiaFSR involved in the cell envelope response to antimicrobials, is directly responsible for a DAP-tolerant phenotype and is likely to negatively affect response to DAP therapy.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Anti-Bacterial Agents / pharmacology
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Bacterial Proteins / genetics*
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Cell Wall / drug effects
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Codon / genetics*
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Daptomycin / pharmacology*
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Drug Resistance, Bacterial / genetics*
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Enterococcus faecium / drug effects*
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Humans
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Microbial Sensitivity Tests / standards
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Sequence Analysis, DNA
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Sequence Deletion / genetics*
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Stem Cells
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Vancomycin / pharmacology
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Vancomycin Resistance
Substances
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Anti-Bacterial Agents
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Bacterial Proteins
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Codon
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Vancomycin
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Daptomycin