Abstract
Reverse mutations in 5 nutritionally-deficient strains of E. coli were studied in detail. Two strains (H12-23 and H88, Sd-4, both deficient for histidine) were found to be "mutagen stable"; that is, it was impossible to increase the rate of their reversion to prototrophy above the spontaneous level by treatment with either u.-v. radiation or MnCl2- Not all histidineless types are mutagen stable, nor is this property limited to histidineless types. Delayed appearance of induced mutants was studied in 3 strains. Each strain has its own characteristic pattern of delay and that this pattern is not a function of the mutagen used in treatment. A hypothesis concerning the mechanism of delayed appearance is discussed. The rate of induction of mutations by u.-v. irradiation differed in each of the 3 strains studied.