PL-promoted transcription of the promoter-proximal N-trp region is insensitive to chloramphenicol in the absence of N function.
When the trp operon is translocated into the early region of lambda phage, transcription originated at the PL promotor is known to be modified by function of the N gene product so that transcription of the operon continues when translation is blocked by nonsense mutations or by ribosomal antibiotics. When N function is deficient in a phage that joins the trp operon to a point distal to the N gene, deleting the tL site, nonsense mutations (Franklin, 1974) or chloramphenicol (Nakamura et al., accompanying paper) again block transcription of the bacterial operon. However, here we report that transcription over about the first 800 nucleotide pairs starting from the PL promotor of the N-trp operon is still insensitive to chloramphenicol even in the absence of N function. The region covers the full N gene and the initial bit of the trp operon.
D002701:Chloramphenicol / Q000494:pharmacology*; D003090:Coliphages / Q000187:drug effects / Q000235:genetics*; D004352:Drug Resistance, Microbial; D005814:Genes, Viral; D009876:Operon; D014158:Transcription, Genetic / Q000187:drug effects*; D014178:Translocation, Genetic; D014364:Tryptophan / Q000096:biosynthesis
D002701:Chloramphenicol; D014364:Tryptophan