Mutagenicity of 3-azido-1,2-propanediol and 9-(3-azido-2-hydroxypropyl)-adenine in repair deficient strains of Escherichia coli

• Published in: Mutation research Vol. 303; no. 1; pp. 1 - 9
• Main Authors: GRUZ, P, JURICEK, M, ZAK, P, VELEMINSKY, J
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.09.1993; Elsevier
• Subjects: 3-Azido-1,2-propanediol; 9-(3-Azido-2-hydroxypropyl)-adenine; Action of physical and chemical agents on bacteria; Ada; Adaptive response; Adenine - analogs & derivatives; Adenine - toxicity; AlkA; Azides - toxicity; Bacteriology; Biological and medical sciences; Dam; DNA Repair; Escherichia coli; Escherichia coli - drug effects; Escherichia coli - genetics; Fundamental and applied biological sciences. Psychology; Gene Expression - drug effects; Microbiology; Molecular Structure; Mutagenicity Tests; Mutagens - toxicity; PolA; Propylene Glycols - toxicity; SOS response; SOS Response (Genetics); TagA; UmuDC; UvrA; 3-Azido-1,2-propanediol; TagA; Escherichia coli; AG; AHPA; Adaptive response; SOS response; Dam; PolA; NaN 3; 9-(3-Azido-2-hydroxypropyl)-adenine; UvrA; UmuDC; AlkA; MNNG; Ada; Mutagenicity testing; Bacteria; SOS function; Enterobacteriaceae; Azido complex; Organic compounds
• ISSN: 0165-7992; 0027-5107
• DOI: 10.1016/0165-7992(93)90002-D

The mutagenicity of two non-aromatic organic azido compounds, 3-azido-1,2-propanediol (AG) and 9-(3-azido-2-hydroxypropyl)-adenine (AHPA), was studied in E. coli repair deficient strains uvrA6, uvrA6 + umuC36, uvrA6 + umuC122::Tn5, polA1, tagA1 + alkA1, ada and dam3. The mutagenicity of both agents was markedly enhanced by defects of UvrABC excinuclease ( uvrA6) and was independent of umC function of the SOS error-prone pathway. Neithr azido compound promoted umuDC operon expression. The mutagenicity of AG in tagA1, alkA1 and ada mutants does not differ from that found in the wild-type strain. The expression of both ada and alkA genes was not elevated by AG. Experiments on polA1 and dam3 mutants suggest that DNA polymerase I as well as the mutHLS mismatch repair pathway does not contribute to the removal of putative DNA lesions induced by AG.