Abstract

The biochemical mechanism of action of viomycin on R. meliloti involved an inhibition of protein synthesis. Adenine and amino acid incorporation into total nucleic acid and cell wall respectively was relatively unaffected. The antibiotic increased the level of 14C in the intracellular pool and "nucleic acids" fraction of cells fed 14C-amino acids but caused no cellular lysis. Mono- and di-valent cations protected cells from growth inhibition by viomycin.A viomycin-resistant mutant was similar to its sensitive parent in rate of uptake of glucose and glutamic acid by both growing and resting cells and in the rate of leakage when preloaded cells were suspended in buffered saline. Viomycin resistance did not appear to be episome-mediated or involve an extracellular degradative enzyme. The ability of TES buffer to eliminate viomycin resistance, coupled with the sensitivity to viomycin of cell-free protein-synthesizing systems derived from both sensitive and resistant cells indicates that resistance is probably the result of a selective reduction in antibiotic permeability.

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