title: Effects of the umuDC, mucAB, and samAB operons on the mutational specificity of chemical mutagenesis in Escherichia coli: II. Base substitution mutagenesis.
abstract: Mutational spectra induced by different classes of chemical mutagens including two ultraviolet-mimetic mutagens, an alkylating agent, intercalators, a crosslinking agent, and base analogs were characterized by means of a set of mutant lacZ genes in E. coli. These strains can be used to detect each of two types of transition and four types of transversion, simply by measuring the number of Lac+ revertant colonies. 4-Nitroquinoline 1-oxide induced G.C-->A.T, G.C-->C.G, or G.C-->T.A changes almost equally, whereas furylfuramide and mitomycin C induced only G.C-->A.T transitions and G.C-->T.A transversions, respectively. No base substitutional mutations were detected by the treatment with 9-aminoacridine. A weak stimulation of G.C-->A.T transitions by ICR-191 was observed. Both the G.C-->A.T and A.T-->G.C transitions were induced by N-methyl-N'-nitro-N-nitrosoguanidine and N4-aminocytidine. 5-Azacytidine was a specific inducer of G.C-->C.G transversions. In addition, a comparative study of mutational specificity was performed in the strains bearing either the umuDC, mucAB, or the samAB operon on a multicopy plasmid. Regardless of the kind of mutagen, G.C-->T.A transversions were greatly potentiated by the introduction of plasmids in the order of pGW1700 (mucAB) > pSE117 (umuDC) > or = pYG8011 (samAB). Besides G.C-->T.A transversions, the introduction of pGW1700, but not pSE117 and pYG8011, enhanced the mutations of A.T-->C.G and A.T-->T.A transversions. The mucAB plasmid also enhanced the G.C-->A.T transitions and G.C-->C.G transversions induced by some mutagens.
authors.affiliation: Institute of Environmental Toxicology, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Nohmi
authors.forename: T
authors.initials: T
authors.lastname: Ohta
mesh_terms: D000585:Aminacrine / Q000031:analogs & derivatives / Q000633:toxicity; D001374:Azacitidine / Q000633:toxicity; D003432:Cross-Linking Reagents / Q000633:toxicity; D003562:Cytidine / Q000031:analogs & derivatives / Q000633:toxicity; D004252:DNA Mutational Analysis; D004269:DNA, Bacterial / Q000187:drug effects*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics; D005668:Furylfuramide / Q000633:toxicity; D007364:Intercalating Agents / Q000633:toxicity; D007763:Lac Operon / Q000187:drug effects* / Q000235:genetics; D008769:Methylnitronitrosoguanidine / Q000633:toxicity; D016685:Mitomycin / Q000633:toxicity; D016297:Mutagenesis, Site-Directed; D009153:Mutagens / Q000633:toxicity*; D009588:Nitrogen Mustard Compounds / Q000633:toxicity; D009876:Operon / Q000235:genetics; D010957:Plasmids; D017354:Point Mutation; D013014:SOS Response, Genetics; D013489:Suppression, Genetic; D014466:Ultraviolet Rays
chemical_list: D003432:Cross-Linking Reagents; D004269:DNA, Bacterial; D007364:Intercalating Agents; D009153:Mutagens; D009588:Nitrogen Mustard Compounds; D005668:Furylfuramide; D008769:Methylnitronitrosoguanidine; D016685:Mitomycin; C038769:N(4)-aminocytidine; D003562:Cytidine; D000585:Aminacrine; C004294:acridine half-mustard; D001374:Azacitidine