MULTIPLICITY REACTIVATION AND REPAIR OF NITROUS ACID-INDUCED LESIONS IN BACTERIOPHAGE-T4

[摘要] HNO2-induced lesions in phage T4 were efficiently repaired by multiplicity reactivation. Mutants defective in genes 32, 46, 47, x and y showed substantially less MR [multiplicity reactivation] of these lesions than wild type. The gene 47 mutant, which showed the least MR of HNO2 lesions, also showed virtually no MR of UV 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. The gene functions employed in MR are probably the same functions used in genetic recombination, and, based on this, a tentative recombinational model for MR is proposed. The mutants defective in genes 32, 46 and 47, which are deficient in recombination, were more sensitive to HNO2 inactivation than wild-type phage upon single infection. In wild-type single infections, about 20% of HNO2-induced lethal lesions may be repaired by a recombinational post-replication form of repair.