In the absence of nucleotide excision repair, the spectra were dominated by G:CrA:T transitions, additional deficiency of the DNA alkyltransferase consistent with the major role of the O 6 -alkylguanine (ATase) encoded by the constitutive ogt gene of miscoding lesion in mutagenesis by alkylating Escherichia coli caused a marked increment in mu-agents. Specific sites for G:CrA:T transitions were tation induction by N-propyl-N-nitrosourea (PNU). recovered more or less frequently in one genetic Irrespective of the presence or the absence of the background versus the others, giving statistically Ogt ATase, little mutagenic response was detected significant differences among the spectra (P õ in Uvr / bacteria in the concentration range 0 -8 10 06 ). We examined the influence of DNA repair mM PNU, indicating that most premutagenic DNA by (A)BC excinuclease and Ogt ATase on the 5lesions induced at these concentrations are effi-flanking base and DNA-strand associated with the ciently recognized and repaired by the nucleotide PNU-induced G:CrA:T transitions. Preferences difexcision repair system. Some increased susceptibil-ferent from those previously reported for the ethylatity to mutagenesis by PNU was detected in Uvr 0 ing (ENU) and methylating (MNU) analogs were Ogt / bacteria, but the Uvr 0 Ogt 0 double mutant detected. We indicate that these differences might exhibited much higher sensitivity. These data sug-be caused by the PNU possibility of giving iso-progest that the Ogt ATase can replace to a great ex-pyl adducts, in addition to the expected n-propyl tent the repair capacity of the (A)BC excinuclease. adducts, and by possible preferences in the initial Forward mutations induced by 6 mM PNU within distribution of these lesions as well as in their rethe initial part of the IacI gene were recovered from pair by the (A)BC excinuclease and the Ogt ATase Uvr / Ogt 0 , Uvr 0 Ogt / , and Uvr 0 Ogt 0 bacteria. A of E. coli. Environ. Mol. Mutagen.