SUMMARY: The increased toxicity of sulphonamides for in the presence of low concentrations (50 100 μM) of purines or purine nucleosides has been confirmed and investigated further. The potentiating effect of a purine was dependent upon the activity of the appropriate phosphoribosyl transferase; a mutant strain was not potentiated by guanine but remained fully sensitive to the addition of adenine. Mutants resistant to the potentiating effect of all purines have been isolated and partially characterized. The site of these mutations has been located in the region between and at minute 83 on the chromosome map. It is suggested that this locus be temporarily designated (potentiation of sulphonamides by purines) because these mutants have unaltered sensitivities to sulphonamides acting alone. Mutations in and did not affect the potentiation of sulphonamides by purines. Hypoxanthine-insensitive strains harbouring λ were as sensitive as the wild-type to the potentiating effect. This result suggests that these lysogens are heterozygous for and that the wild-type allele is dominant. It is probable that is a regulatory gene, affecting some rate-limiting step in the biosynthesis of methionine.


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