On the glucose effect in acridine-induced frameshift mutagenesis in Escherichia coli.
Log-phase cells of E. coli growing in defined minimal media were washed, exposed to acridines in the same minimal salts solution, and plated to select for Nad+ revertants. At low mutagen concentration, treatment in the presence of the carbon source to which the cells were adapted resulted in a decrease in revertant yield of several orders of magnitude compared with the yield in the absence of a carbon source. At high mutagen concentration, however, a carbon source present during treatment caused a 2- to 150-fold increase in revertant yield (depending on the mutagen, the carbon source, and on the genetic background of the strain). In a strain lacking adenylate cyclase, acridine mutagenesis was not abolished under the experimental conditions used in this study, and the addition of cAMP during mutagenic treatment had no effect. In mismatch repair-deficient strains, the presence of glucose during treatment with low mutagen concentration did not cause a decrease in revertant yield as drastic as in the wild type. From the results reported here, we conclude that the glucose effect in acridine mutagenesis is due to an enhancement of mismatch repair.
Pons
F W
FW
Institut für Mikrobiologie, J.W. Goethe-Universität, Frankfurt-am-Main, F.R.G.
Müller
P
P
D000585:Aminacrine / Q000494:pharmacology*; D000609:Aminoacridines / Q000494:pharmacology*; D000242:Cyclic AMP / Q000494:pharmacology; D004260:DNA Repair; D004734:Energy Metabolism; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology*; D005990:Glycerol / Q000494:pharmacology; D009154:Mutation / Q000187:drug effects*; D011190:Potassium Cyanide / Q000494:pharmacology
D000609:Aminoacridines; D000585:Aminacrine; D000242:Cyclic AMP; D005947:Glucose; D011190:Potassium Cyanide; D005990:Glycerol