The involvement of a putative two component system PA2797-PA2798 in P. aeruginosa aminoglycoside resistance
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Pseudomonas aeruginosa is an opportunistic pathogen, being able to live in a diverse environmental niche. It possesses several resistance mechanisms, including a highly impermeable outer membrane and multiple RND-family efflux pumps, against a variety of antimicrobials, including aminoglycosides. P. aeruginosa causes a variety of infections in individuals, especially those with compromised immune system. Chronic lung infection in cystic fibrosis (CF) patients is an example of such. The most common antibiotic used today to treat the P. aeruginosa pulmonary infection in CF patients belongs to one of the major antibiotic families, aminoglycosides. Due to constant exposure of P. aeruginosa to aminoglycosides, this bacterium has gradually developed high level of resistance to aminoglycosides through the acquisition and selection of numerous chromosomal mutations. Previous P. aeruginosa transposon mutant library screen identified genes contributing to aminoglycoside resistance, including an atypical regulatory system, PA2797-PA2798. The array study on P. aeruginosa K767 ΔPA2798 determined possible pathways by which PA2797-PA2798 was connected to aminoglycoside resistance. A series of in-frame gene deletion (anr), gene cloning (rpoS, anr, rpsP operon), double deletion (rpoS and anr in K767 ΔPA2798), q-RT PCR (pslA, lexA, recN, rpsP operon), and a growth assay (K767, K767 ΔPA2797, K767 ΔPA2798) was performed to examine a possible connection between PA2797-PA2798, and RpoS, Anr, oxidative stress response, temperature stress response, and ribosomal proteins. Although the aforementioned experiments were performed successfully, none of them could identify a potential pathway through which PA2797-PA2798 was connected to aminoglycoside resistance.