Metabolic abnormalities of 2,6-diaminopurine-resistant mutants of Salmonella typhimurium.

Abstract

SummaryResistance to 2,6-diaminopurine in Salmonella typhimurium resulted in 2 phenotypically distinguishable mutants. The mutant dap-r-3 differed from the mutant dap-r-6 in its cross-resistance to other purine analogues and also in its ability to allow the satellite growth of the parent sensitive strain LT-2 when plated in presence of inhibitory concentrations of adenine or DAP. The satellite phenomenon could be explained by the fact that adenine and uracil, which were excreted by the mutant dap-r-3, prevented the inhibition of the wild type by DAP and adenine respectively. Excretions of these compounds were not directly responsible for the resistance to DAP, since the dap-r-3 type mutation could also be demonstrated in auxotrophic strains incapable of synthesizing adenine or uracil de novo. The mutation to a dap-r-3 type in a purine requiring auxotroph resulted in an additional defect characterized by poor growth response to all the purines.