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MexT, an activator protein for the MexEF-OprN multi-drug efflux pump, eliminates induction of the MexAB-OprM multi-drug efflux pump in the presence of N- -L-homoserine lactone



MexT, an activator protein for the MexEF-OprN multi-drug efflux pump, eliminates induction of the MexAB-OprM multi-drug efflux pump in the presence of N- -L-homoserine lactone



Abstracts of the General Meeting of the American Society for Microbiology 103: K-080



Background: Pseudomonas aeruginosa is an opportunistic pathogen that causes infections in immunocompromised hosts and colonizes in the lungs of individuals with cystic fibrosis. This organism shows broad resistance to structurally and functionally dissimilar antibiotics. The nfxC-type cells of P. aeruginosa producing the MexEF-OprN efflux pump exhibits resistance to fluoroquinolines, chloramphenicol and tetracycline and hypersusceptibility to most classical beta-lactam antibiotics. This antibiotic resistance profile could only be observed in the presence of functional MexT, a positive regulator of the mexEF-oprN operon. We investigated the molecular mechanism of how the nfxC mutation causes the beta-lactam hypersusceptibility. Methods and Reslts: When transcription of the mexAB-oprM operon was measured with a mexA::lacZ reporter, the nfxC-type mutant showed a repressed level of beta-galactosidase activity compared with that in cells without a nfxC mutation. On the other hand, expression of the mexAB-oprM operon was higher in the stationary growth phase when the quorum sensing autoinducer N-(3-butyryl)-L-homoserine lactone (C4-HSL) accumulates, suggesting that C4-HSL may be an inducer of the mexAB-oprM operon. This assumption was verified by demonstrating that exogenously added C4-HSL strongly induced expression of MexAB-OprM. This C4-HSL-mediated transcription of the mexAB-oprM operon was repressed by the introduction of plasmid-borne mexT. We conclud that beta-lactam hypersusceptibility in the nfxC-type cells is caused by MexT-mediated down regulation of MexAB-OprM expression, and suggest that mexT-mediated expression of MexEF-OprN cross talks with C4-HSL-mediated regulation of MexAB-OprM expression.

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Accession: 035305086

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