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.