An endonuclease specific for single-stranded DNA selectively damages the genomic DNA and induces the SOS response.
A plasmid carrying the bacteriophage T7.3 endonuclease gene under the control of the lacUV5 promoter could be maintained in the transcriptionally active state only in recA+ strains. In recA- strains, endonuclease induction resulted in extensive degradation of the genomic DNA and cell death. In sharp contrast, the plasmid DNA remained intact in the supercoiled form. In recA+ strains, the recA protein levels were increased and the SOS functions of the host were activated, as shown by measurements of recA protein synthesis and prophage induction. These results indicate that in normal undisrupted and non-irradiated cells, enzymatic nucleolytic damage can induce the SOS response and can be controlled by the DNA repair system of the host. In addition, the higher sensitivity of the genomic DNA to the single-strand-specific endonuclease relative to the plasmid suggests that the two molecules differ in their physiological states and most likely in their degree of single-stranded content.
D002470:Cell Survival; D004260:DNA Repair; D004277:DNA, Single-Stranded / Q000378:metabolism*; D004591:Electrophoresis, Polyacrylamide Gel; D004790:Enzyme Induction; D007763:Lac Operon; D011938:Rec A Recombinases / Q000096:biosynthesis; D014764:Viral Proteins / Q000096:biosynthesis / Q000378:metabolism*
C041424:0.3 protein, Enterobacteria phage T7; D004277:DNA, Single-Stranded; D014764:Viral Proteins; D011938:Rec A Recombinases