Lipiarmycin-resistant ribonucleic acid polymerase mutants of Bacillus subtilis.
Lipiarmycin inhibited the activity of deoxyribonucleic acid-dependent ribonucleic acid (RNA) polymerase in vitro. We showed that inhibition was due to interference by lipiarmycin with the activity of sigma-containing molecules of RNA polymerase. Transcription by core enzyme was relatively resistant to the drug, but addition of sigma led to highly drug-sensitive RNA synthesis. We isolated lipiarmycin-resistant mutants of Bacillus subtilis and characterized them genetically and biochemically. Drug-resistant mutants contained an altered RNA polymerase that was resistant to the drug in vitro. By separation and mixed reconstitution of core and sigma fractions of mutant and wild-type RNA polymerase, we showed that lipiarmycin resistance in one mutant strain was a property of the core fraction. Genetic mapping experiments indicated that at least two lpm mutants are located between loci determining rifampin resistance and streptolydigin resistance.
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001412:Bacillus subtilis / Q000187:drug effects / Q000201:enzymology*; D012321:DNA-Directed RNA Polymerases / Q000096:biosynthesis* / Q000378:metabolism; D004352:Drug Resistance, Microbial; D009154:Mutation; D011067:Poly dA-dT / Q000378:metabolism; D012329:RNA, Bacterial / Q000096:biosynthesis; D013698:Templates, Genetic; D014158:Transcription, Genetic / Q000187:drug effects
D000900:Anti-Bacterial Agents; D012329:RNA, Bacterial; D011067:Poly dA-dT; D012321:DNA-Directed RNA Polymerases