title: Isolation of Escherichia coli rpoB mutants resistant to killing by lambda cII protein and altered in pyrE gene attenuation.
abstract: Escherichia coli mutants simultaneously resistant to rifampin and to the lethal effects of bacteriophage lambda cII protein were isolated. The sck mutant strains carry alterations in rpoB that allow them to survive cII killing (thus the name sck), but that do not impair either the expression of cII or the activation by cII of the lambda promoters pE and pI. The sck-1, sck-2, and sck-3 mutations modify transcription termination. The growth of lambda, but not of the N-independent lambda variant, lambda nin-5, is hindered by these mutations, which act either alone or in concert with the bacterial nusA1 mutation. In contrast to their effect on lambda growth, the three mutations reduce transcription termination in bacterial operons. The E. coli pyrE gene, which is normally regulated by attenuation, is expressed constitutively in the mutant strains. The sck mutations appear to prevent pyrE attenuation by slowing the rate of transcriptional elongation of the pyrE leader sequence. The sck-6 mutation, unlike the other sck mutations, neither increases pyrE expression nor inhibits the ability of lambda to suppress transcription termination. Instead, the sck-6 mutation blocks the growth of the lambda variants lambda nin-5 and lambda red-3.
mesh_terms: D010582:Bacteriophage lambda / Q000235:genetics*; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development; D005798:Genes, Bacterial; D005816:Genetic Complementation Test; D009154:Mutation; D010957:Plasmids; D012293:Rifampin / Q000494:pharmacology; D014157:Transcription Factors / Q000502:physiology*; D014158:Transcription, Genetic; D014764:Viral Proteins
chemical_list: D014157:Transcription Factors; D014764:Viral Proteins; C039000:cII protein, bacteriophage lambda; D012293:Rifampin