ArticlePLoS genetics2015
Competition between VanU(G) repressor and VanR(G) activator leads to rheostatic control of vanG vancomycin resistance operon expression.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- On the Low Abundance of Antibiotic Resistance Genes in Bacteriophage Genomes and Their Random Acquisition via Specialized Transduction.Genome biology and evolution · 2026Article
- The HtrA chaperone monitors sortase-assembled pilus biogenesis in Enterococcus faecalis.PLoS genetics · 2024Article
- Histidine kinase-mediated cross-regulation of the vancomycin-resistance operon in Clostridioides difficile.Molecular microbiology · 2024Article
- The Regulations of Essential WalRK Two-Component System onJournal of clinical medicine · 2023Review
- VanG- and D-Ala-D-Ser-dependent peptidoglycan synthesis and vancomycin resistance in Clostridioides difficile.Molecular microbiology · 2022Article
- Genetic Mechanisms of Vancomycin Resistance inAntibiotics (Basel, Switzerland) · 2022Review
- Regulation of Resistance in Vancomycin-Resistant Enterococci: The VanRS Two-Component System.Microorganisms · 2021Review
- Molecular mechanisms of vancomycin resistance.Protein science : a publication of the Protein Society · 2020Review
- The Enterococcus: a Model of Adaptability to Its Environment.Clinical microbiology reviews · 2019Review
- Characterization of a Linezolid- and Vancomycin-ResistantFrontiers in microbiology · 2019Article
- Functional Dissection of the CroRS Two-Component System Required for Resistance to Cell Wall Stressors in Enterococcus faecalis.Journal of bacteriology · 2016Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterococcus faecalis BM4518 is resistant to vancomycin by synthesis of peptidoglycan precursors ending in D-alanyl-D-serine. In the chromosomal vanG locus, transcription of the resistance genes from the PYG resistance promoter is inducible and, upstream from these genes, there is an unusual three-component regulatory system encoded by the vanURS(G) operon from the P(UG) regulatory promoter. In contrast to the other van operons in enterococci, the vanG operon possesses the additional vanU(G) gene which encodes a transcriptional regulator whose role remains unknown. We show by DNase I footprinting, RT-qPCR, and reporter proteins activities that VanU(G), but not VanR(G), binds to P(UG) and negatively autoregulates the vanURS(G) operon and that it also represses PYG where it overlaps with VanR(G) for binding. In clinical isolate BM4518, the transcription level of the resistance genes was dependent on vancomycin concentration whereas, in a ΔvanUG mutant, resistance was expressed at a maximum level even at low concentrations of the inducer. The binding competition between VanU(G) and VanR(G) on the P(YG) resistance promoter allowed rheostatic activation of the resistance operon depending likely on the level of VanR(G) phosphorylation by the VanS(G) sensor. In addition, there was cross-talk between VanS(G) and VanR'(G), a VanR(G) homolog, encoded elsewhere in the chromosome indicating a sophisticated and subtle regulation of vancomycin resistance expression by a complex two-component system.
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