Induction of the SOS response by ICR191 does not influence frameshift mutagenesis at the hisC3076 marker of Salmonella typhimurium.
Reversion of the Salmonella typhimurium frameshift marker hisC3076 by ICR191 and 9-aminoacridine in rec+ and recA1 backgrounds was examined using the standard plate-reversion assay. For both compounds, the level of reversion observed in the recA strain is significantly greater than in the rec+ strain. Thus reversion of hisC3076 is not recA-dependent, but is recA-modulated. The ability of a mutagen (or mutagenic treatment) to induce the recA lexA-dependent SOS response does not therefore imply that mutagenic effects will also be recA-dependent.
D000585:Aminacrine / Q000031:analogs & derivatives / Q000494:pharmacology*; D000609:Aminoacridines / Q000494:pharmacology* / Q000633:toxicity; D001483:Base Sequence; D004260:DNA Repair / Q000187:drug effects*; D005798:Genes, Bacterial; D006639:Histidine / Q000235:genetics; D009154:Mutation / Q000187:drug effects*; D009588:Nitrogen Mustard Compounds / Q000494:pharmacology*; D009876:Operon; D012486:Salmonella typhimurium / Q000187:drug effects / Q000235:genetics*; D013329:Structure-Activity Relationship
D000609:Aminoacridines; D009588:Nitrogen Mustard Compounds; D006639:Histidine; D000585:Aminacrine; C004294:acridine half-mustard