Repair of DNA double-strand breaks in Escherichia coli K12 requires a functional recN product.
Mutation of the recN gene of Escherichia coli in a recBC sbcB genetic background blocks conjugational recombination and confers increased sensitivity to UV light and mitomycin C. The basis for this phenotype was investigated by monitoring the properties associated with recN mutations in otherwise wild-type strains. It was established that recN single mutants are almost fully resistant to UV irradiation, and that there is no detectable defect in repair of UV lesions by excision, error-prone, or recombinational mechanisms. However, recN mutations confer sensitivity to mitomycin C and ionizing radiation both in wild-type and recB sbcB strains. The sensitivity to ionizing radiation is correlated with a deficiency in the capacity to repair DNA double-strand breaks by a UV inducible mechanism. Recombinant lambda phages that complement the recombination and repair defects of recN recBC sbcB mutants have been identified, and the recN gene has been cloned from these phages into a low copy-number plasmid.
D001426:Bacterial Proteins / Q000235:genetics*; D004260:DNA Repair; D004262:DNA Restriction Enzymes; D004307:Dose-Response Relationship, Radiation; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000528:radiation effects; D005796:Genes; D005798:Genes, Bacterial; D005838:Genotype; D016685:Mitomycin; D008937:Mitomycins / Q000633:toxicity; D009154:Mutation; D010957:Plasmids; D014466:Ultraviolet Rays
D001426:Bacterial Proteins; D008937:Mitomycins; D016685:Mitomycin; D004262:DNA Restriction Enzymes