ArticleAntimicrobial agents and chemotherapy2010
A single mutation in enzyme I of the sugar phosphotransferase system confers penicillin tolerance to Streptococcus gordonii.
Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Antimicrobial Activity of Aurisin A AgainstInternational journal of molecular sciences · 2026Article
- Nanomotion technology: an innovative method to study cell metabolism inJournal of medical microbiology · 2024Article
- In-patient evolution of a high-persisterProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Inhibitory Effect of Monoterpenoid Glycosides Extracts from Peony Seed Meal onInternational journal of environmental research and public health · 2022Article
- Market forces determine the distribution of a leaky function in a simple microbial community.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Assessing Pseudomonas aeruginosa Persister/antibiotic tolerant cells.Methods in molecular biology (Clifton, N.J.) · 2014Article
- Loss of function of the gdpP protein leads to joint β-lactam/glycopeptide tolerance in Staphylococcus aureus.Antimicrobial agents and chemotherapy · 2012Article
- The Lcn972 bacteriocin-encoding plasmid pBL1 impairs cellobiose metabolism in Lactococcus lactis.Applied and environmental microbiology · 2011Article
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Authors and funding
6 authors.
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Abstract
Tolerance is a poorly understood phenomenon that allows bacteria exposed to a bactericidal antibiotic to stop their growth and withstand drug-induced killing. This survival ability has been implicated in antibiotic treatment failures. Here, we describe a single nucleotide mutation (tol1) in a tolerant Streptococcus gordonii strain (Tol1) that is sufficient to provide tolerance in vitro and in vivo. It induces a proline-to-arginine substitution (P483R) in the homodimerization interface of enzyme I of the sugar phosphotransferase system, resulting in diminished sugar uptake. In vitro, the susceptible wild-type (WT) and Tol1 cultures lost 4.5 and 0.6 log(10) CFU/ml, respectively, after 24 h of penicillin exposure. The introduction of tol1 into the WT (WT P483R) conferred tolerance (a loss of 0.7 log(10) CFU/ml/24 h), whereas restitution of the parent sequence in Tol1 (Tol1 R483P) restored antibiotic susceptibility. Moreover, penicillin treatment of rats in an experimental model of endocarditis showed a complete inversion in the outcome, with a failure of therapy in rats infected with WT P483R and the complete disappearance of bacteria in animals infected with Tol1 R483P.
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