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Remarkably, D. radiodurans cells rendered ionizing radiation-sensitive by a polA mutation are fully complemented by expression of the polA gene from ionizing radiation-sensitive E. coli [24].
Paradoxically, however, IR-, UV-, and mitomycin-C (MMC -sensitive D. radiodurans polA MMC -sensitivelly complementeD.by expradioduransthe polA gene fromutantsR-sensitive Escherichiareoli [4].
A positively selected polA paralog set might also explain the results of Gutman et al. [ 38], who showed that ionizing-radiation-sensitive D. radiodurans polA mutants are fully complemented by expression of the polA gene from the relatively ionizing-radiation sensitive E. coli.
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In both cases, the repair deficiency was fully complemented in Pol β null cells expressing recombinant Pol β.
The attenuation of prcBA-TetON was fully complemented with doxy.
This robust MMC-induced mutator phenotype was fully complemented by the DinB-expressing plasmid (Fig. 4B).
H2O2 hypersensitivity was statistically significant (p<0.05, based on two-way ANOVA with Bonferroni post-test), and was fully complemented by the MutS-expressing plasmid (pmutS).
Furthermore, the hemolysis defect of the original ausA mutant on blood agar was fully complemented by the plasmid carrying the sae operon [ΔausA pCL-sae) in Fig. 3A].
Consistent with results discussed above, this defect was fully complemented by the DinB-expressing plasmid, providing further support for a role for DinB (Fig. 3B).
Hypermutability of the mutS strain was fully complemented by plasmid pmutS (Table 1), which expresses the P. aeruginosa MutS protein from its native promoter.
Sensitivity of the dinB strain was statistically significant at concentrations ≥200 nM H2O2 (p<0.05), and was fully complemented by the DinB-expressing plasmid, pAR101.
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