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Identification of GntR as regulator of the glucose metabolism in Pseudomonas aeruginosa
- Daddaoua, A., Corral‐Lugo, A., Ramos, J.‐L., Krell, Tino
- Environmental microbiology 2017 v.19 no.9 pp. 3721-3733
- DNA, DNA-directed RNA polymerase, Escherichia coli, Pseudomonas aeruginosa, bacteria, binding sites, consensus sequence, exotoxins, genes, gluconates, glucose, metabolism, models, virulence
- In contrast to Escherichia coli, glucose metabolism in pseudomonads occurs exclusively through the Entner‐Doudoroff (ED) pathway. This pathway, as well as the three routes to generate the initial ED pathway substrate, 6‐phosphogluconate, is regulated by the PtxS, HexR and GtrS/GltR systems. With GntR (PA2320) we report here the identification of an additional regulator in Pseudomonas aeruginosa PAO1. GntR repressed its own expression as well as that of the GntP gluconate permease. In contrast to PtxS and GtrS/GltR, GntR did not modulate expression of the toxA gene encoding the exotoxin A virulence factor. GntR was found to bind to promoters PgₙₜR and PgₙₜP and the consensus sequence of its operator was defined as 5′‐AC‐N‐AAG‐N‐TAGCGCT‐3′. Both operator sites overlapped with the RNA polymerase binding site and we show that GntR employs an effector mediated de‐repression mechanism. The release of promoter bound GntR is induced by gluconate and 6‐phosphogluconate that bind with similar apparent affinities to the GntR/DNA complex. GntR and PtxS are paralogous and may have evolved from a common ancestor. The concerted action of four regulatory systems in the regulation of glucose metabolism in Pseudomonas can be considered as a model to understand complex regulatory circuits in bacteria.