ArticleNucleic acids research2025
MexR and NalD are pyocyanin-responsive transcriptional repressors of the efflux pump MexAB-OprM in Pseudomonas aeruginosa.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Transcriptional regulation drives heteroresistance inmSystems · 2026Article
- From low- to high-level resistance: dynamic transcriptional adaptations and efflux pump amplification in cefiderocol-stressedFrontiers in microbiology · 2026Article
- Broadly Defined Antibiotic Adjuvants forThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Review
- Lipid Droplet Degradation Through Lipophagy in Aurantiochytrium limacinum mh0186.Marine biotechnology (New York, N.Y.) · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
The secondary metabolite pyocyanin (PYO) significantly enhances the antibiotic resistance of Pseudomonas aeruginosa by inducing expression of the resistance-nodulation-cell division efflux systems. However, the mechanisms underlying the initial derepression and subsequent upregulation of MexAB-OprM, regulated by multiple transcriptional repressors, remain unclear. Here, we demonstrate that MexR and NalD, the transcriptional repressors of MexAB-OprM, function as PYO receptors, with dissociation constants of 5.17 and 7.03 μM, respectively. Electrophoretic mobility shift assays show that PYO binding to MexR and NalD induces their dissociation from the mexA promoter, leading to the derepression of mexAB-oprM expression. Structural simulations and mutagenesis assays identified residues F17, R21, and M61 in MexR, as well as R66, N129, and F132 in NalD, as critical for PYO binding. Additionally, PYO and the MexAB-OprM substrate novobiocin competitively bind to MexR and NalD, suggesting that PYO can attenuate the effectiveness of clinical antibiotics by triggering mexAB-oprM expression. Furthermore, PYO establishes a negative feedback regulatory mechanism through NalD, which also functions as a transcriptional activator of phenazine biosynthesis genes, thereby restricting PYO overproduction to maintain cellular homeostasis. This regulatory pathway provides an energy-efficient survival strategy for P. aeruginosa in hostile environments.
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