Xanthomonas campestris pv. campestris, a soil-borne plant-pathogenic bacterium, is exposed to multiple stresses in the environment and during interaction with a host plant. The roles of hydrogen peroxide (H(2) O(2) )-protective genes (katA, katG, and ahpC) and a peroxide sensor/transcription regulator (oxyR) in the viability of X. campestris pv. campestris at an elevated temperature were evaluated. The single katA and katG mutants showed moderate decreased survival after the heat treatment, while the double katA-katG and oxyR mutants were the most vulnerable to the heat treatment compared with a wild-type strain. However, ahpC provided no protective function against the heat treatment. Flow cytometric analysis revealed an increased accumulation of peroxide in cells treated with heat. Altogether, the data revealed a crucial role of genes in the H(2) O(2) detoxification system for protection against lethal heat shock in X. campestris pv. campestris.
The exposure of Xanthomonas campestris pv. campestris to sublethal concentrations of a sodium hypochlorite (NaOCl) solution induced the expression of genes that encode peroxide scavenging enzymes within the OxyR and OhrR regulons. Sensitivity testing in various X. campestris mutants indicated that oxyR, katA, katG, ahpC, and ohr contributed to protection against NaOCl killing. The pretreatment of X. campestris cultures with oxidants, such as hydrogen peroxide (H2O2), t-butyl hydroperoxide, and the superoxide generator menadione, protected the bacteria from lethal concentrations of NaOCl in an OxyR-dependent manner. Treating the bacteria with a low concentration of NaOCl resulted in the adaptive protection from NaOCl killing and also provided cross-protection from H2O2 killing. Taken together, the results suggest that the toxicity of NaOCl is partially mediated by the generation of peroxides and other reactive oxygen species that are removed by primary peroxide scavenging enzymes, such as catalases and AhpC, as a part of an overall strategy that protects the bacteria from the lethal effects of NaOCl.
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