Glucose inhibition of mutagenesis by 9-aminoacridine in Salmonella typhimurium.
Back mutation to prototrophy of the hisC3076 marker of Salmonella typhimurium has been measured following treatment with 9-aminoacridine (9AA) under conditions in which growth is either permitted or not permitted. Cells treated with 9AA in buffer (i.e. under conditions in which little or no replication was possible) were found to respond well to 9AA-induced mutagenesis. This remained true whether or not the plating medium contained trace amounts of histidine to allow residual replication of His- cells (as for example in the Ames test); yields of His+ mutants were also about the same regardless of whether the plating medium contained glucose or glycerol as the sole carbon source. By contrast, 9AA-induced mutagenesis was essentially abolished when cells were treated in buffer containing 1% glucose (i.e. under conditions which strongly favoured replication). Glucose inhibition of 9AA-induced mutagenesis began to be apparent at glucose concentrations of about 0.02%, whilst total abolition was observed at about 0.2%. In addition, glucose inhibition was found to be dependent on the concentration of 9AA, the induced mutation rate increasing at levels of up to 100-150 micrograms/ml of 9AA and then declining steeply at higher levels. Further kinetic studies indicated that glucose could depress the 9AA-induced mutation rate significantly even in cells exposed to the mutagen for up to 18 min prior to the addition of glucose, whilst inhibition of 9AA mutagenesis by glucose was both temporary and reversible.
Kopsidas
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G
Department of Microbiology, LaTrobe University, Bundoora, Vic., Australia.
MacPhee
D G
DG
D000585:Aminacrine / Q000494:pharmacology*; D004260:DNA Repair / Q000187:drug effects; D005947:Glucose / Q000494:pharmacology*; D016296:Mutagenesis / Q000187:drug effects*; D012486:Salmonella typhimurium / Q000187:drug effects / Q000235:genetics*
D000585:Aminacrine; D005947:Glucose