Restriction in vivo. V. Introduction of SOS functions in Escherichia coli by restricted T4 phage DNA, and alleviation of restriction by SOS functions.
Degradation products of restricted T4 DNA induced filamentation, mutagenesis, and to a lesser extent, synthesis of recA protein in wild type cells but not in recA, lexA or recBC mutants of Escherichia coli. We conclude that the structural damage to the DNA caused by restriction cleavage and exonuclease V degradation can induce SOS functions. Degradation of restricted nonglycosylated T4 DNA by exonuclease V delayed cell division and induced filament formation and mutagenesis in lexA+ but not in lexA- cells. Delay of cell division was also dependent upon recA and recBC functions. Such degradation of DNA also dramatically increased mutagenesis in tif- Sfi- cells at 42 degrees. The synthesis of recA protein continued in the restricting host after infection by the monglucosylated T4 phage, but enhanced synthesis is not induced to the extent seen in SOS induced tif- cells grown at 42 degrees. We also found that restriction of nonglycosylated T4 was alleviated in UV irradiated cells. The UV induced alleviation of rgl and  rK restriction depended upon post irradiation protein synthesis and was not observed in recA, lexA or recBC mutants.
D004260:DNA Repair; D004269:DNA, Bacterial / Q000235:genetics* / Q000528:radiation effects; D004279:DNA, Viral / Q000494:pharmacology*; D004926:Escherichia coli / Q000235:genetics; D010641:Phenotype; D011995:Recombination, Genetic; D013604:T-Phages / Q000235:genetics*; D014364:Tryptophan / Q000235:genetics; D014466:Ultraviolet Rays
D004269:DNA, Bacterial; D004279:DNA, Viral; D014364:Tryptophan