An Investigation into the Role of trkH Gene Knock-out in the Development of Gentamicin-Resistance in E. coli

Atypical gene mutations, such as mutated trkH gene, contribute to the worldwide increase of antibiotic resistance in bacteria. trkH influences the intracellular concentration of potassium ions by encoding TrkH, an intracellular potassium-ion transporter thus mutations can prevent antibiotic uptake. Since mutated trkH is not easily identified as they are not normally involved in the resistance evolution, it is a threat towards the potency of gentamicin. Research into the role of trkH in the gentamicin-resistance evolution in E. coli may contribute to the development of novel antibiotic therapies to combat resistance. The MIC and resistance induction revealed bacterial growth at high gentamicin concentrations. Growth curve analysis indicated strains exposed to gentamicin were in an extended lag phase; but unexposed strains had a normal growth activity. This was mirrored in the disk-diffusion and reversion rate tests wherein gentamicin-exposed strains were unable to grow in the presence of antibiotics but grew on agars without; meanwhile, all strains unexposed to antibiotic grew sufficiently. The varied results were confirmed by statistical analysis, which revealed the trkH gene to pose an influence in the metabolism of E. coli. Besides the gene’s influence, environmental factors were uncovered to have a possible significant role on the metabolism of E. coli. Moreover, resistance evolution may not necessarily progress to complete resistance. Heteroresistance, tolerance, and disruptions in cell composition and/or surface were investigated to be involved in the adaptation to antibiotic presence.