Potentiation by purines of the growth-inhibitory effects of sulphonamides on Escherichia coli K12 and the location of the gene which mediates this effect.

The increased toxicity of sulphonamides for Escherichia coli in the presence of low concentrations (50-100 microM) 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 gpt 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 oriC and asnA at minute 83 on the E. coli chromosome map. It is suggested that this locus be temporarily designated psp (potentiation of sulphonamides by purines) because these mutants have unaltered sensitivities to sulphonamides acting alone. Mutations in PurA, purR and folB did not affect the potentiation of sulphonamides by purines. Hypoxanthine-insensitive strains harbouring lambda asn20 were as sensitive as the wild-type to the potentiating effect. This result suggests that these lysogens are heterozygous for psp and that the wild-type allele is dominant. It is probable that psp is a regulatory gene, affecting some rate-limiting step in the biosynthesis of methionine.