Oxygen exposure increases resistance of Desulfovibrio vulgaris Hildenborough to killing by hydrogen peroxide
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Inactivation of PerR by oxidative stress and a corresponding increase in expression of the perR regulon genes is part of the oxidative stress defense in a variety of anaerobic bacteria. Diluted anaerobic, nearly sulfide-free cultures of mutant and wild-type Desulfovibrio vulgaris (105–106 colony-forming units/ml) were treated with 0 to 2,500 μM H2O2 for only 5 min to prevent readjustment of gene expression. Survivors were then scored by plating. The wild type and perR mutant had 50% survival at 58 and 269 μM H2O2, respectively, indicating the latter to be 4.6-fold more resistant to killing by H2O2 under these conditions. Significantly increased resistance of the wild type (38-fold; 50% killing at 2188 μM H2O2) was observed if cells were pretreated with full air for 30 min, conditions that did not affect cell viability. The resistance of the perR mutant increased less (4.6-fold; 50% killing at 1230 μM H2O2), when similarly pretreated. Interestingly, no increased resistance of either was achieved by exposure with 10.6 μM H2O2 for 30 min, the highest concentration that could be used without killing the cells. Hence, in environments with low D. vulgaris biomass only the presence of external O2 effectively activates the perR regulon. As a result, mutant strains lacking one of the perR regulon genes ahpC, dvu0772, rbr1 or rbr2 displayed decreased resistance to H2O2 stress only following pretreatment with air.
KeywordsSulfate-reducing bacteria Hydrogen peroxide Oxidative stress PerR Rubrerythrin Desulfovibrio
Colony forming units
Polymerase chain reaction
This work was supported by an NSERC Discovery Grant to GV. GV also acknowledges salary support from an NSERC Industrial Research Chair Award.
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