Reciprocal regulation of resistance-nodulation-division efflux systems and the Cpx two-component system in Vibrio cholerae.
Identifieur interne : 000223 ( France/Analysis ); précédent : 000222; suivant : 000224Reciprocal regulation of resistance-nodulation-division efflux systems and the Cpx two-component system in Vibrio cholerae.
Auteurs : Dawn L. Taylor [États-Unis] ; X Renee Bina [États-Unis] ; Leyla Slamti [France] ; Matthew K. Waldor [États-Unis] ; James E. Bina [États-Unis]Source :
- Infection and immunity [ 1098-5522 ] ; 2014.
Descripteurs français
- KwdFr :
- Données de séquences moléculaires, Liaison génétique, Mutation, Protéines bactériennes (génétique), Protéines bactériennes (métabolisme), Protéines de transport (génétique), Protéines de transport (métabolisme), Protéines de transport membranaire, Régulation de l'expression des gènes bactériens (physiologie), Séquence nucléotidique, Vibrio cholerae (génétique), Vibrio cholerae (métabolisme).
- MESH :
- génétique : Protéines bactériennes, Protéines de transport, Vibrio cholerae.
- métabolisme : Protéines bactériennes, Protéines de transport, Vibrio cholerae.
- physiologie : Régulation de l'expression des gènes bactériens.
- Données de séquences moléculaires, Liaison génétique, Mutation, Protéines de transport membranaire, Séquence nucléotidique.
English descriptors
- KwdEn :
- Bacterial Proteins (genetics), Bacterial Proteins (metabolism), Base Sequence, Carrier Proteins (genetics), Carrier Proteins (metabolism), Gene Expression Regulation, Bacterial (physiology), Genetic Linkage, Membrane Transport Proteins, Molecular Sequence Data, Mutation, Vibrio cholerae (genetics), Vibrio cholerae (metabolism).
- MESH :
- chemical , genetics : Bacterial Proteins, Carrier Proteins.
- chemical , metabolism : Bacterial Proteins, Carrier Proteins.
- genetics : Vibrio cholerae.
- metabolism : Vibrio cholerae.
- physiology : Gene Expression Regulation, Bacterial.
- Base Sequence, Genetic Linkage, Membrane Transport Proteins, Molecular Sequence Data, Mutation.
Abstract
The Cpx two-component regulatory system has been shown in Escherichia coli to alleviate stress caused by misfolded cell envelope proteins. The Vibrio cholerae Cpx system was previously found to respond to cues distinct from those in the E. coli system, suggesting that this system fulfills a different physiological role in the cholera pathogen. Here, we used microarrays to identify genes that were regulated by the V. cholerae Cpx system. Our observations suggest that the activation of the V. cholerae Cpx system does not induce expression of genes involved in the mitigation of stress generated by misfolded cell envelope proteins but promotes expression of genes involved in antimicrobial resistance. In particular, activation of the Cpx system induced expression of the genes encoding the VexAB and VexGH resistance-nodulation-division (RND) efflux systems and their cognate outer membrane pore protein TolC. The promoters for these loci contained putative CpxR consensus binding sites, and ectopic cpxR expression activated transcription from the promoters for the RND efflux systems. CpxR was not required for intrinsic antimicrobial resistance, but CpxR activation enhanced resistance to antimicrobial substrates of VexAB and VexGH. Mutations that inactivated VexAB or VexGH efflux activity resulted in the activation of the Cpx response, suggesting that vexAB and vexGH and the cpxP-cpxRA system are reciprocally regulated. We speculate that the reciprocal regulation of the V. cholerae RND efflux systems and the Cpx two-component system is mediated by the intracellular accumulation of an endogenously produced metabolic by-product that is normally extruded from the cell by the RND efflux systems.
Url:
DOI: 10.1128/IAI.00025-14
PubMed: 24799626
Affiliations:
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pubmed:24799626Le document en format XML
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<front><div type="abstract" xml:lang="en">The Cpx two-component regulatory system has been shown in Escherichia coli to alleviate stress caused by misfolded cell envelope proteins. The Vibrio cholerae Cpx system was previously found to respond to cues distinct from those in the E. coli system, suggesting that this system fulfills a different physiological role in the cholera pathogen. Here, we used microarrays to identify genes that were regulated by the V. cholerae Cpx system. Our observations suggest that the activation of the V. cholerae Cpx system does not induce expression of genes involved in the mitigation of stress generated by misfolded cell envelope proteins but promotes expression of genes involved in antimicrobial resistance. In particular, activation of the Cpx system induced expression of the genes encoding the VexAB and VexGH resistance-nodulation-division (RND) efflux systems and their cognate outer membrane pore protein TolC. The promoters for these loci contained putative CpxR consensus binding sites, and ectopic cpxR expression activated transcription from the promoters for the RND efflux systems. CpxR was not required for intrinsic antimicrobial resistance, but CpxR activation enhanced resistance to antimicrobial substrates of VexAB and VexGH. Mutations that inactivated VexAB or VexGH efflux activity resulted in the activation of the Cpx response, suggesting that vexAB and vexGH and the cpxP-cpxRA system are reciprocally regulated. We speculate that the reciprocal regulation of the V. cholerae RND efflux systems and the Cpx two-component system is mediated by the intracellular accumulation of an endogenously produced metabolic by-product that is normally extruded from the cell by the RND efflux systems.</div>
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