title: Effects of DNA repair deficiency on the mutational specificity in the lacZ gene of Escherichia coli.
abstract: The mutational specificities of various chemical mutagens were compared in isogenic E. coli strains with different DNA repair capabilities (wild-type, uvrA, umuC, and uvrA umuC) in a reversion assay employing a set of mutant lacZ genes that can detect two types of transitions, four types of transversions, and five kinds of specific frameshift events. A uvrA derivative was more sensitive than the wild-type strain to 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone for +1G, -1G, -2(C-G), +1A and -1A frameshifts, G.C-->A.T transitions, and G.C-->T.A transversions. In a uvrA background, G.C-->T.A transversions and +1G, +1A, and -1A frameshifts appeared to be umuC-dependent, while G.C-->A.T transitions were not. N-Ethyl-N'-nitro-N-nitrosoguanidine was more mutagenic in a uvrA background for five kinds of frameshifts and G.C-->A.T transitions, but not for G.C-->T.A, A.T-->C.G, and A.T-->G.C base substitutions. A.T-->C.G transversions were totally dependent on umuC gene function. For the investigation of mutational specificities induced by frameshift mutagens, an rfa mutation was additionally introduced. The rfa strain responded to 2-nitrofluorene, which induced primarily -2(C-G) frameshift mutations. In an rfa uvrA background, benzo[a]pyrene induced +1G, -1G, +1A, and -1A frameshifts. 2-Aminoanthracene induced +1G, -1G, and +1A, but not -1A, frameshifts, with -1G frameshifts predominating. Ethidium bromide induced only two types of frameshifts, -1G and +1A. Frameshifts induced by ICR-170 were independent of umuC gene function, while those by induced 1-nitropyrene were partly umuC-dependent.
authors.affiliation: Laboratory of Genetic Toxicology, Institute of Environmental Toxicology, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Watanabe-Akanuma
authors.forename: T
authors.initials: T
authors.lastname: Ohta
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000609:Aminoacridines; D000873:Anthracenes / Q000633:toxicity; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D001564:Benzo(a)pyrene / Q000633:toxicity; D011088:DNA Ligases / Q000172:deficiency; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000378:metabolism; D004259:DNA-Directed DNA Polymerase; D004926:Escherichia coli / Q000187:drug effects; D029968:Escherichia coli Proteins; D004996:Ethidium; D005449:Fluorenes / Q000633:toxicity; D016368:Frameshift Mutation; D005663:Furans / Q000633:toxicity; D005798:Genes, Bacterial; D016695:Glycosyltransferases; D007763:Lac Operon / Q000187:drug effects*; D008727:Methotrexate / Q000633:toxicity; D008769:Methylnitronitrosoguanidine / Q000031:analogs & derivatives / Q000633:toxicity; D016296:Mutagenesis; D009152:Mutagenicity Tests; D009153:Mutagens / Q000633:toxicity; D009588:Nitrogen Mustard Compounds / Q000633:toxicity; D017354:Point Mutation; D011721:Pyrenes; D013045:Species Specificity; D013489:Suppression, Genetic; D001616:beta-Galactosidase / Q000235:genetics
chemical_list: D000609:Aminoacridines; D000873:Anthracenes; D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; D029968:Escherichia coli Proteins; D005449:Fluorenes; D005663:Furans; D009153:Mutagens; D009588:Nitrogen Mustard Compounds; D011721:Pyrenes; C091910:acridine mustard; D008769:Methylnitronitrosoguanidine; C019499:2-nitrofluorene; D001564:Benzo(a)pyrene; C013525:ENNG; C054121:3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone; C006593:2-anthramine; C078202:UmuC protein, E coli; D016695:Glycosyltransferases; C080934:lipooligosaccharide 1,5-heptosyltransferase; D004259:DNA-Directed DNA Polymerase; C055218:UmuD protein, E coli; D001616:beta-Galactosidase; C068631:UvrA protein, E coli; D000251:Adenosine Triphosphatases; D011088:DNA Ligases; D004996:Ethidium; C032668:1-nitropyrene; D008727:Methotrexate