Fig. 1: Contribution of Pol IV to oxodGTP mutagenesis and gene inactivation.

A Mutation rates for the wild-type (WT), mutS^β (S^β), dinB (D) and mutS^β dinB (S^βD) strains treated ( + PQ) or not (- PQ) with paraquat (40 independent cultures). B Mutation rates for the mutT (T), mutT mutS^β (TS^β), mutT dinB (TD) and mutT mutS^β dinB (TS^βD) strains (20 independent cultures). Mutation rates to ciprofloxacin resistance (Cip^r) per replication and 95% confidence limits were calculated as described in Materials and Methods. Error bars represent the upper and lower 95% confidence limits. Data were statistically analyzed using the likelihood ratio test. C Representative images of luminescent Cip^r clones from the WT, S^β, D and S^βD strains carrying the chromosomal transcriptional fusion of the mexCD-oprJ promoter to the luxCDABE operon. D NfxB inactivation in Cip^r clones from the WT, S^β, D and S^βD strains. Luminescence intensity was measured in exponentially growing cultures of individual Cip^r clones (25–30). The relative luminescence level was calculated as the ratio between the luminescence intensity in the Cip^r clone and the corresponding parental strain. Clones showing luminescence increases of up to 6-, 12- and 18-fold were arbitrarily categorized as expressing NfxB variants with low, medium and high inactivation levels, respectively. Values are the mean from three independent experiments. Results were evaluated using one-way ANOVA and Tukey tests.