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Mutagenesis. 1997 Jan;12(1):23-8.

Effects of nitrous acid treatment on the survival and mutagenesis of Escherichia coli cells lacking base excision repair (hypoxanthine-DNA glycosylase-ALK A protein) and/or nucleotide excision repair.

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  • 1Groupe R├ęparation des L├ęsions Radio- et Chimio-Induites, URA 147 CNRS. Institut Gustave Roussy, Villejuif, France.


Deoxyinosine occurs in DNA by spontaneous deamination of adenine or by incorporation of dITP during replication. Hypoxanthine residues (HX) are mutagenic and give rise to A-T-->G-C transition. They are substrates for the Escherichia coli product of the alkA gene, the 3-methyl-adenine-DNA glycosylase II (ALK A protein). In mammalian cells and in yeast, HX is excised by the counterpart of ALK A protein, the ANPG or the MAG proteins respectively. We have investigated in vivo the contribution of the alkA gene to counteract the lethal and/or mutagenic effects of HX residues induced by nitrous acid treatment. Using an E.coli strain allowing the detection of A-T-->G-C transition, we show that the alkA mutant has a slightly increased spontaneous rate of mutation and about the same sensitivity when treated with HNO2 as compared with the wild-type strain. Using the E.coli alkA mutant carrying a multicopy plasmid expressing the ALK A protein or the ANPG protein, we barely observe any effect of HNO2 treatment on sensitivity and mutation rate of the bacteria. In contrast, the same experiment performed with a uvrA- strain, deficient in nucleotide excision repair (NER), shows that this mutant is extremely sensitive to HNO2 treatment. Furthermore, the sensitivity and the spontaneous mutation rate observed in the double mutant alkA- uvrA- are almost identical to those of the uvrA- mutant. Hence, NER has the major role in vivo for the repair of lethal and mutagenic lesions induced by HNO2.

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