Regulation of the dnaQ gene of Escherichia coli in mutants expressing the SOS regulon constitutively.
Current models for the mechanism of SOS mutagenesis in E. coli propose the involvement of a new or modified DNA polymerase III holoenzyme in error-prone replicative bypass of bulky DNA lesions assuming an inhibited or excluded 3'----5' proofreading exonuclease function of DNA polymerase. By promotor fusion to galK, gene fusion to lacZ and Sl analysis the in vivo regulation of dnaQ coding the proofreading subunit of DNA polymerase III holoenzyme was analyzed under conditions of induced or constitutive SOS expression. The results presented here clearly show that, at least on the level of gene expression no regulatory event seems to contribute to the assumed decrease of proofreading activity during SOS mediated error-prone bypassing of bulky lesions. On the contrary, an increase in dnaQ gene expression was observed following treatment with some SOS inducing agents which produces bulky DNA lesions.
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Wissenschaftsbereich Genetik der Martin-Luther-Universität, Halle, DDR.
D004258:DNA Polymerase III / Q000235:genetics*; D004926:Escherichia coli / Q000235:genetics*; D015964:Gene Expression Regulation, Bacterial; D005798:Genes, Bacterial; D009154:Mutation; D013014:SOS Response, Genetics; D014158:Transcription, Genetic
D004258:DNA Polymerase III