ArticleFrontiers in microbiology2015
Transposon Mutagenesis Identifies Novel Genes Associated with Staphylococcus aureus Persister Formation.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
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- Eradication ofAntibiotics (Basel, Switzerland) · 2022Article
- Transcript Profiling of Nitroxoline-Treated Biofilms Shows Rapid Up-regulation of Iron Acquisition Gene Clusters.ACS infectious diseases · 2022Article
- Mutations in respiratory complex I promote antibiotic persistence through alterations in intracellular acidity and protein synthesis.Nature communications · 2022Article
- Dynamic PET-facilitated modeling and high-dose rifampin regimens forScience translational medicine · 2021Article
- cydA, spdC, and mroQ are novel genes involved in the plasma coagulation of Staphylococcus aureus.Microbiology and immunology · 2021Article
- Antibiotic tolerance is associated with a broad and complex transcriptional response in E. coli.Scientific reports · 2021Article
- MazF toxin causes alterations in Staphylococcus aureus transcriptome, translatome and proteome that underlie bacterial dormancy.Nucleic acids research · 2021Article
- Identification of population of bacteria from culture negative surgical site infection patients using molecular tool.BMC surgery · 2021Article
- TheFrontiers in microbiology · 2021Article
- Involvement of Small Colony Variant-Related Heme Biosynthesis Genes inFrontiers in microbiology · 2021Article
- Studying Bacterial Persistence: Established Methods and Current Advances.Methods in molecular biology (Clifton, N.J.) · 2021Article
- A Quantitative Survey of Bacterial Persistence in the Presence of Antibiotics: Towards Antipersister Antimicrobial Discovery.Antibiotics (Basel, Switzerland) · 2020Article
- Persistence ofFrontiers in microbiology · 2020Review
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Pathogenic bacterial persisters are responsible for the recalcitrance of chronic and persistent infections to antimicrobial therapy. Although the mechanisms of persister formation and survival have been widely studied in Escherichia coli, persistence mechanisms in Staphylococcus aureus remain largely unknown. Here, we screened a transposon mutant library of a clinical methicillin-resistant Staphylococcus aureus(MRSA)strain, USA500 (ST8), under antibiotic pressure and identified 13 genes whose insertion mutations resulted in a defect in persistence. These candidate genes were further confirmed by evaluating the survival of the mutants upon exposure to levofloxacin and several other stress conditions. We found 13 insertion mutants with significantly lower persister numbers under several stress conditions, including sdhA, sdhB, ureG, mnhG1, fbaA, ctaB, clpX, parE, HOU_0223, HOU_0587, HOU_2091, HOU_2315, and HOU_2346, which mapped into pathways of oxidative phosphorylation, TCA cycle, glycolysis, cell cycle, and ABC transporters, suggesting that these genes and pathways may play an important role in persister formation and survival. The newly constructed knockout strains of ureG, sdhA and sdhB and their complemented strains were also tested for defect in persisters following exposure to levofloxacin and several other stress conditions. The results from these experiments were consistent with the screening results, which indicated that deletion of these genes in MRSA USA500 leads to persister defect. These findings provide novel insights into the mechanisms of persister formation and survival in S. aureus and offer new targets for the development of persister-directed antibiotics for the improved treatment of chronic and persistent infections.
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