Abstract
Summary
The mechanism of excretion of adenine by the mutant dap-r-3 of Salmonella typhimurium selected for resistance to DAP was studied. The mechanism for control of purine biosynthesis by feedback inhibition is unaffected in this mutant as indicated by (1) inhibition of AICA synthesis in sulfadiazineinhibited prototrophic strains dap-r-3 and LT-2 by hypoxanthine and adenine; and (2) inhibition of AICA synthesis by adenine and its nucleoside in nonproliferating suspensions of Escherichia coli B 96/1/dap, a DAP-resistant mutant derived from a purine requiring auxotroph B 96/1 resembling dap-r-3 mutant in its properties. In general, more adenine was required for feedback inhibition in the resistant mutant than in the parent strain. The differences have been ascribed to poor utilization of adenine by the resistant strain.
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