Recognition of altered deoxyribonucleic acid in recombination.
Kinetics of inactivation of transduction by phage P1bt which had been treated with ultraviolet light (UV) or nitrous acid (NA) was examined. With Escherichia coli B/r (radiation-resistant), low doses of UV increased transduction frequency, but the frequency was exponentially inactivated by higher doses. Little initial stimulus was observed in strain B(s-1) (radiation-sensitive). The final rate of decay was the same as in B/r. The initial stimulus of transduction in B/r was probably a consequence of increased recombination resulting from dark repair. It was estimated that another nucleotide within 1000 nucleotide pairs had to be damaged by UV to prevent a given nucleotide from successful transduction. The NA dose response was the same for the two strains. An initial stimulus of transduction was followed by exponential decline. The UV-repair enzymes missing in B(s-1) were not required for repair of NA-induced damage to transducing or lytic phage DNA. Low recovery of new mutations in the transductants showed that mutagen-induced damage to transducing DNA was excluded from recombinant chromosomes. The few recovered mutants may have resulted from "normal" error in recombination.
D003090:Coliphages; D004269:DNA, Bacterial; D004926:Escherichia coli / Q000528:radiation effects; D005827:Genetics, Microbial; D007700:Kinetics; D008967:Molecular Biology; D009154:Mutation; D009609:Nitrous Oxide / Q000494:pharmacology; D011830:Radiation Effects; D011831:Radiation Genetics; D011995:Recombination, Genetic; D012762:Shigella dysenteriae; D014161:Transduction, Genetic; D014466:Ultraviolet Rays
D004269:DNA, Bacterial; D009609:Nitrous Oxide