Recombinational repair of alkylation lesions in phage T4

Abstract
Treatment of phage T4-host adsorption complexes by MNNG1 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 temperatures, proved to be substantially more sensitive to MNNG at such temperatures than wild-type phage. In addition, the recombination defective mutants x m(uvsX) and y 10(y) were more 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 subject to multiplicity reactivation, but mutants defective in genes 46 or 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 on 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 substantially to induced mutagenesis.

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