Treatment of phage T4-host adsorption complexes by MNNG increased recombination between two rII markers by about three-fold. Temperature sensitive mutants defective in genes 32, 46 and 47, which cause reductions in recombination at semirestrictive temperature, proved to be substantially more sensitive to MNNG at such temperatures than wild-type phage. In addition, the recombination defective mutants xm(uvsX) and y10(y) were sensitive to MNNG than wild-type, whereas mutants defective in genes 45 and denV, which are apparently not involved in recombination, were not MNNG sensitive. These findings suggest that a recombination pathway involving the products of genes 32, 46, 47, uvsX and y is employed in repairing MNNG-induced lethal lesions. This mechanism is effective in cells infected by single phage, implying post-replication recombinational repair between daughter chromosomes. MNNG-induced lesions are subjects to multiplicity reactivation, but mutants defective in genes 46 to 47 showed the same degree of multiplicity reactivation as wild-type phage. The gene 32 and gene 47 recombination defective mutants were tested for their effects of MNNG-induced reversion of an rII marker. No reduction in induced reversion was found. Thus, it appears that the postulated recombinational repair pathway employing the products of genes 32 and 47 does not contribute substanitally to induced mutagenesis.