engleski

Modulation of genotoxic response in Salmonella typhimurium by the overexpression of Escherichia coli 3-methyladenine-DNA glycosylase II (AlkA)

Salmonella typhimurium exhibits a weak adaptive response when compared to E. coli. The weak induction results from poor transcriptional activation by the self-methylated Ada protein. It harbours only a constitutive glycosylase activity, lacking an equivalent of the alkA gene of E. coli which codes for an inducible 3-methylpurine-DNA glycosylase II. Thus, all S. typhimurium strains are much more sensitive to alkylating agents than E. coli ones.DMS, a classic SN2 alkylating mutagen methylates purines at positions N3 and N7, primarily inducing GC-AT transitions. However, the applied doses were very low, considering biological relevance, allowing the minimal cell survival to 20 percent and assuring the possibility of screening for histidine prototrophic (his+) mutants. Our interest was to see whether in conditions of overproduced ALkA protein the deficiency of an inducible glycosylase activity could be suppressed, decreasing toxicity and mutation induction in the S. typhimurium strains which differ in their nucleotide excision repair capabilities.

Salmonella typhimurium ; genotoxicity ; Escherichia coli ; 3 methyladenine-DNA-glycosylase II (AlkA)

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