AI Article Synopsis
- Exposure to the aminoglycoside paromomycin (PAR) triggers the expression of PA3720-armR and the mexAB-oprM efflux operon, but the induction of mexAB-oprM by PAR is not reliant on armR.
- Various aminoglycosides enhance mexAB-oprM expression, which requires the presence of the amgRS locus that regulates the bacterium's response to envelope stress.
- While both aminoglycosides and the thiol-active reagent diamide induce mexAB-oprM through AmgR, this efflux system does not seem to provide resistance against these stressors.
Article Abstract
Exposure of P. aeruginosa to the aminoglycoside (AG) paromomycin (PAR) induced expression of the PA3720-armR locus and the mexAB-oprM multidrug efflux operon that AmgR controls, although PAR induction of mexAB-oprM was independent of armR. Multiple AGs promoted mexAB-oprM expression and this was lost in the absence of the amgRS locus encoding an aminoglycoside-activated envelope stress-responsive 2-component system (TCS). Purified AmgR bound to the mexAB-oprM promoter region consistent with this response regulator directly regulating expression of the efflux operon. The thiol-active reagent, diamide, which, like AGs, promotes protein aggregation and cytoplasmic membrane damage also promoted AmgRS-dependent mexAB-oprM expression, a clear indication that the MexAB-OprM efflux system is recruited in response to membrane perturbation and/or circumstances that lead to this. Despite the AG and diamide induction of mexAB-oprM, however, MexAB-OprM does not appear to contribute to resistance to these agents.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6173428 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0205036 | PLOS |
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