Multiplicity reactivation and repair of nitrous acid-induced lesions in bacteriophage T4

Nitrous acid-induced lesions in phage T4 were shown to be efficiently repaired by multiplicity reactivation. Mutants defective in genes 32, 46, 47, x and y showed substantially less MR ² of these lesions than wild type. The gene 47 mutant, which showed the least MR of nitrous acid lesions, also showed virtually no MR of ultraviolet lesions. Mutations in genes 30, 44 and v did not affect MR of nitrous acid-induced lesions. Each of the mutations which lowered MR was shown previously to reduce recombination. Our results suggest that the gene functions employed in MR are the same functions used in genetic recombination, and, based on this, we propose a tentative recombinational model for MR.The mutants defective in genes 32, 46 and 47, which are deficient in recombination, were shown to be more sensitive to nitrous acid inactivation than wild-type phage upon single infection. Our results indicate that, in wild-type single infections, about 20% of nitrous acid-induced lethal lesions may be repaired by a recombinational post-replication form of repair.