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• W1873163513 startingPage "1267" @default.
• W1873163513 abstract "Summary In G ram‐negative bacteria, multidrug efflux pumps are responsible for the extrusion of chemicals that are deleterious for growth. Some of these efflux pumps are induced by endogenously produced effectors, while abiotic or biotic signals induce the expression of other efflux pumps. In P seudomonas putida , the TtgABC efflux pump is the main antibiotic extrusion system that respond to exogenous antibiotics through the modulation of the expression of this operon mediated by TtgR . The plasmid‐encoded TtgGHI efflux pump in P . putida plays a minor role in antibiotic resistance in the parental strain; however, its role is critical in isogenic backgrounds deficient in TtgABC . Expression of ttgGHI is repressed by the TtgV regulator that recognizes indole as an effector, although P . putida does not produce indole itself. Because indole is not produced by P seudomonas , the indole‐dependent antibiotic resistance seems to be part of an antibiotic resistance programme at the community level. P seudomonas putida recognizes indole added to the medium or produced by E scherichia coli in mixed microbial communities. Transcriptomic analyses revealed that the indole‐specific response involves activation of 43 genes and repression of 23 genes. Indole enhances not only the expression of the TtgGHI pump but also a set of genes involved in iron homeostasis, as well as genes for amino acid catabolism. In a ttgABC ‐deficient P . putida , background ampicillin and other bactericidal compounds lead to cell death. Co‐culture of E . coli and P . putida Δ ttgABC allowed growth of the P . putida mutant in the presence of ampicillin because of induction of the indole‐dependent efflux pump." @default.
• W1873163513 created "2016-06-24" @default.
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• W1873163513 creator A5070634527 @default.
• W1873163513 date "2014-01-23" @default.
• W1873163513 modified "2023-10-17" @default.
• W1873163513 title "Interspecies signalling:<i>Pseudomonas putida</i>efflux pump TtgGHI is activated by indole to increase antibiotic resistance" @default.
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• W1873163513 doi "https://doi.org/10.1111/1462-2920.12368" @default.
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