High Sensitivity of the rpiAB Escherichia coli Mutants to Antibiotics Is Mediated by Participation of the Deo-Operon in Creation of Ribose-5-Phosphate Futile Cycle

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Abstract
Previously we demonstrated that disruption of ribose-5-phosphate biosynthesis in the pentose phosphate pathway increases the sensitivity of E. coli bacteria to a broad spectrum of antibiotics, and this sensitivity can be suppressed by deletion of the deoB gene. In this study, we demonstrated that antibiotic sensitivity can also be suppressed by disruption of the apt gene, which, along with the deoDB genes, constitutes the salvage pathway for purine base uptake. We suggest that in the rpiAB mutant, these genes, together with the prs gene encoding PRPP synthesis, create a futile cycle, which convers ATP to AMP and PPi. Inactivation each of these genes leads to suppression of the antibiotic sensitivity phenotype of the rpiAB mutant and to restoration of energy status.
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