Suppressors specific for frameshift mutations have been studied. Of 21 frameshift mutations of the histidine operon selected for study, 13 gave rise to ICR† † Abbreviations used: ICR-191, 2-chloro-6-methoxy-9-(3-(2-chloroethyl) aminopropylamino) acridine dihydrochloride; DES, diethylsulfate; 2-AP, 2-aminopurine nitrate; NG, N-methyl-N′-nitro-N-nitrosoguanidine; INT, 2-p-iodophenyl-3-p-nitrophenyl-5-phenyltetrazolium chloride.-induced external suppressors. Five of these mutants also gave rise to nitrosoguanidine-induced suppressors. Two frameshift mutations in the tryptophan operon were found which could be suppressed externally along with certain his frameshift mutations. Most of the externally suppressible mutations ( 12 15) are those tentatively classified as (+1) frameshifts. Forty-eight independent suppressor mutations were placed in 9 groups on the basis of their ability to suppress 13 his frameshift mutations. The 13 suppressible mutations are apparently of two general types. No cross-suppression of mutations of these two types has been observed. The efficiency of suppression was estimated for at least one suppressor from each of 8 groups. The efficiency of suppression ranges from 1% to about 15%.
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