Mutagenicity of 3-azido-1,2-propanediol and 9-(3-azido-2-hydroxypropyl)-adenine in repair deficient strains of Escherichia coli
Language English Country Netherlands Media print
Document type Journal Article
PubMed
7690900
DOI
10.1016/0165-7992(93)90002-d
PII: 0165-7992(93)90002-D
Knihovny.cz E-resources
- MeSH
- Adenine analogs & derivatives toxicity MeSH
- Azides toxicity MeSH
- Escherichia coli drug effects genetics MeSH
- Gene Expression drug effects MeSH
- Molecular Structure MeSH
- Mutagens toxicity MeSH
- DNA Repair * MeSH
- Propylene Glycols toxicity MeSH
- SOS Response, Genetics MeSH
- Mutagenicity Tests MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- 9-(3-azido-2-hydroxypropyl)adenine MeSH Browser
- Adenine MeSH
- azidoglycerol MeSH Browser
- Azides MeSH
- Mutagens MeSH
- Propylene Glycols MeSH
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 umuC function of the SOS error-prone pathway. Neither azido compound promoted umuDC operon expression. The mutagenicity of AG in tag A1, 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.
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