PCP failed, however, to induce mexAB-oprM in a mexR deletion strain, indicating that MexR was required for this, although PCP did not modulate MexR binding to mexAB-oprM promoter-containing DNA in vitro. While modulation of MexR by the ArmR anti-repressor explains the upregulation of mexAB-oprM in nalC mutants hyperexpressing PA3720- armR, the induction of mexAB-oprM expression by PCP is not wholly explainable by PCP induction of PA3720- armR and subsequent ArmR modulation of MexR, inasmuch as armR deletion mutants still showed PCP-inducible mexAB-oprM expression. The NalC binding site was localized to an inverted repeat (IR) sequence upstream of PA3720- armR and overlapping a promoter region whose transcription start site was mapped. PCP's induction of PA3720- armR resulted from its direct modulation of NalC, the repressor's binding to PA3720- armR promoter-containing DNA as seen in electromobility shift assays (EMSAs) being obviated in the presence of this agent. Pentachlorophenol (PCP) induced expression of the NalC repressor-regulated PA3720- armR operon and the MexR repressor-controlled mexAB-oprM multidrug efflux operon of Pseudomonas aeruginosa.
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