Altered transcriptional termination in a rifampicin-resistant mutant of Escherichia coli which inhibits the growth of bacteriophage T7.
A spontaneous rifampicin-resistant mutant of E. coli K12, RpoB26, which inhibits the growth of bacteriophage T7 has been isolated. The mutation is an RNA polymerase mutation; it also restores the wild-type effect of polar mutations in a rho-deficient strain, probably by restoring transcriptional termination. The efficiency of plating (e.o.p.) of wild-type T7, and of some early region deletion and point mutants of T7 tested, is reduced on RpoB26 by a factor of 10(-4). However, some deletion mutants are inhibited more severely (up to 10(-7) on RpoB26. We argue that these differences may reflect variations in the frequency of transcriptional termination before gene 1, an essential gene which codes for the T7 RNA polymerase (Summers and Siegel 1970; Chamberlin et al. 1970). We also present data which suggest that the product of a late T7 gene plays a role, by some interaction with the product of gene 1, in the inhibition of T7 in RpoB26. We suggest that different levels of expression of gene 1 may lead to different degrees of inhibition of T7 strains in RpoB26.
D012321:DNA-Directed RNA Polymerases / Q000378:metabolism; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000235:genetics*; D005814:Genes, Viral; D009154:Mutation; D010641:Phenotype; D014176:Protein Biosynthesis; D012293:Rifampin / Q000494:pharmacology*; D013604:T-Phages / Q000254:growth & development
D012321:DNA-Directed RNA Polymerases; D012293:Rifampin