ArticleAntimicrobial agents and chemotherapy2011
Off-target gene regulation mediated by transcriptional repressors of antimicrobial efflux pump genes in Neisseria gonorrhoeae.
Article in Antimicrobial agents and chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- MtrR Regulates a Major Lytic Transglycosylase (Microorganisms · 2026Article
- Functional characterization of the gonococcal polyphosphate pseudo-capsule.PLoS pathogens · 2023Article
- Transcriptional regulation of theMicrobiology (Reading, England) · 2022Review
- Structures of Neisseria gonorrhoeae MtrR-operator complexes reveal molecular mechanisms of DNA recognition and antibiotic resistance-conferring clinical mutations.Nucleic acids research · 2021Article
- MarR family proteins are important regulators of clinically relevant antibiotic resistance.Protein science : a publication of the Protein Society · 2020Review
- Mutations in Neisseria gonorrhoeae grown in sub-lethal concentrations of monocaprin do not confer resistance.PloS one · 2018Article
- Proteomics, Bioinformatics and Structure-Function Antigen Mining For Gonorrhea Vaccines.Frontiers in immunology · 2018Review
- The genes that encode the gonococcal transferrin binding proteins, TbpB and TbpA, are differentially regulated by MisR under iron-replete and iron-depleted conditions.Molecular microbiology · 2016Article
- The Transcriptional Repressor, MtrR, of the mtrCDE Efflux Pump Operon of Neisseria gonorrhoeae Can Also Serve as an Activator of "off Target" Gene (glnE) Expression.Antibiotics (Basel, Switzerland) · 2015Article
- Overproduction of the MtrCDE efflux pump in Neisseria gonorrhoeae produces unexpected changes in cellular transcription patterns.Antimicrobial agents and chemotherapy · 2015Article
- Antimicrobial resistance in Neisseria gonorrhoeae in the 21st century: past, evolution, and future.Clinical microbiology reviews · 2014Review
- Article
- RND multidrug efflux pumps: what are they good for?Frontiers in microbiology · 2013Article
- Emergence of multidrug-resistant, extensively drug-resistant and untreatable gonorrhea.Future microbiology · 2012Review
- Antibiotic resistance in Neisseria gonorrhoeae: origin, evolution, and lessons learned for the future.Annals of the New York Academy of Sciences · 2011Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
DNA-binding proteins that control expression of drug efflux pump genes have been termed "local regulators" as their encoding gene is often located adjacent to the gene(s) that they regulate. However, results from recent studies indicate that they can control genes outside efflux pump-encoding loci, which we term as being "off target." For example, the MtrR repressor was initially recognized for its ability to repress transcription of the mtrCDE-encoded efflux pump operon in the strict human pathogen Neisseria gonorrhoeae, but recent results from genetic and microarray studies have shown that it can control expression of nearly 70 genes scattered throughout the chromosome. One of the off-target MtrR-repressed genes is glnA, which encodes glutamine synthetase. Herein, we confirm the capacity of MtrR to repress glnA expression and provide evidence that such repression is due to its ability to negatively influence the binding of a second DNA-binding protein (FarR), which activates glnA. FarR was previously recognized as a transcriptional repressor of the farAB-encoded efflux pump operon. Thus, two DNA-binding proteins previously characterized as repressors of genes encoding efflux pumps that contribute to gonococcal resistance to antimicrobials can act in an opposing manner to modulate expression of a gene involved in basic metabolism.
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Registered trials
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