On the mechanism of inhibitory effect of violamycin antibiotics on the transcription by bacteriophage T3-induced RNA polymerase.
The effect of three components of the anthracycline antibiotic violamycin on the transcription of bacteriophage T3 DNA by bacteriophage T3-induced RNA polymerase has been investigated in a cell-free system. The glycosides of violamycin BI possess the highest inhibitory activity, whereas those of violamycin BII and violamycin A show a reduced inhibitory effect. Concentrations of violamycin BI depressing the incorporation of (3H)UMP into RNA chains have only a slight effect on the binding of the T3 RNA polymerase to T3 DNA and on the incorporation of GTP as the first nucleotide. This shows that the primary target of the antibiotic is not the initiation of the RNA synthesis. The binding of violamycin BI to T3 DNA causes a strong reduction of the elongation rate of the RNA chains.
D000617:Aminoglycosides / Q000494:pharmacology; D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial / Q000378:metabolism*; D012321:DNA-Directed RNA Polymerases / Q000378:metabolism*; D010441:Peptide Chain Elongation, Translational / Q000187:drug effects; D013604:T-Phages / Q000187:drug effects / Q000378:metabolism*; D014158:Transcription, Genetic / Q000187:drug effects*
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; C010806:violamycins; D012321:DNA-Directed RNA Polymerases