We described earlier the isolation of lfl25 mutation reducing the frequency of lysogenization of mutant cells by phage lambda (LycA phenotype). The mutation is mapped at present in the rpoC gene coding for the beta' subunit of bacterial RNA polymerase and named rpoC90. It is dominant and causes decrease in pools of some branched amino acids, pyrimidines and thiamine (vitamin B1) in mutant cells. Combination of rpoC90 mutation with some Rif-r mutations strengthens both the LycA phenotype and deficiency in metabolites mentioned above. Such combination was shown to also cause a defect in antitermination (or increases the efficiency of termination) of transcription on the DNA of lambdoid phage phi 434. This defect may indicate the possible mechanism of changes in the regulation of different bacterial operons induced by rpoC90 mutation.