The mutagenicity of 7-bromomethylbenz[ a]anthracene, a reactive arylalkylating carcinogen, was investigated in several strains of E. coli WP2, using reversion from tryptophan auxotrophy ( ochre trpE locus) as a measure of induced mutation. WP2, the wild-type with respect to DNA repair, was more resistant to the cytotoxic effects of 7-bromomethylbenz[ a]anthracene than WP2 uvrA, WP2 exrA, or WP2 uvrAexrA, the D 37 doses of carcinogen being 22, 5, 8, and 1 μg/ml respectively. Mutagenesis in WP2 was observed only at doses in excess of the D Q , whereas in WP2 uvrA mutation was linearly related to dose throughout the range studies. No mutation was detectable in WP2 exrA or WP2 uvrAexrA even at doses which resulted in 95% and 99.9% lethality respectively. It was concluded that an intact Exr function was an absolute requirement for the induction of mutation by 7-bromomethylbenz[ a]anthracene and that excision-repair was very efficient in removing premutational lesios. The use of [ 3 H]7- bromomethylbenz[a] anthracene at high specific radioactivity enabled the quantitation of mutation as a function of the extent of reaction of the mutagen with cellular macromolecules. Extent of reaction with DNA, RNA and protein was linearly related to dose, binding to DNA being 3 times that to RNA and 20 times that to protein. There was a linear relationship between binding and mutation in WP2 uvrA and the effective target size for Exr-mediated mutation in this system was of the order of 0.04 nucleotides. Having established that the n umber of 7-bromomethylbenz[ a]anthracene-induced mutants increased linearly with successive cell generations and, by use of T4 ochre427, that about 30% of the mutants scored were true revertants, it was estimated that the Exr pathway incorporates productive errors into the bacterial genome with a frequency of the order of 2.10 −3.