Topoisomerase involvement in multiplicity reactivation of phage T4.
The products of phage T4 genes 39, 52 and probably 60 have been previously characterized as forming a type II DNA topoisomerase. Other evidence suggested that this topoisomerase promotes normal initiation of DNA replication, and that when it is defective its loss is partially compensated for by the host gyrase. We present evidence here that mutants defective in genes 39, 52 and 60 have reduced ability to carry out multiplicity reactivation (MR, a form of recombinational repair) of phage DNA damaged either by mitomycin C (MMC) or psoralen plus near-UV light (PUVA). We also observed that there is not extensive superhelicity in the intracellular phage DNA either in the presence or absence of the phage topoisomerase. This tends to rule out the possibility that the topoisomerase influences MR by controlling the general superhelicity of the phage DNA. The dependence of MR on topoisomerase could occur in several possible ways. However, we favor the explanation that the lesions are bypassed by a postreplication recombinational repair process that is influenced by the topoisomerase through its role in initiating replication.
D004260:DNA Repair; D004264:DNA Topoisomerases, Type I / Q000235:genetics*; D011564:Furocoumarins / Q000494:pharmacology; D005796:Genes; D005814:Genes, Viral; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology; D009154:Mutation; D011995:Recombination, Genetic; D013604:T-Phages / Q000235:genetics*
D011564:Furocoumarins; D008937:Mitomycins; D016685:Mitomycin; D004264:DNA Topoisomerases, Type I