OxyR mediated compensatory expression between ahpC and katA and the significance of ahpC in protection from hydrogen peroxide in Xanthomonas campestris

katA and ahpC, encoding monofunctional catalase and alkyl hydroperoxide reductase, respectively, play important protective roles against peroxide toxicity in Xanthomonas campestris pv. phaseoli (Xp). The expression of both katA and ahpC is controlled by the global peroxide sensor and transcriptional...

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Main Authors: Nisanart Charoenlap, Warawan Eiamphungporn, Nopmanee Chauvatcharin, Supa Utamapongchai, Paiboon Vattanaviboon, Skorn Mongkolsuk
Other Authors: Chulabhorn Research Institute
Format: Article
Published: 2018
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Online Access:https://repository.li.mahidol.ac.th/handle/123456789/16310
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Institution: Mahidol University
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Summary:katA and ahpC, encoding monofunctional catalase and alkyl hydroperoxide reductase, respectively, play important protective roles against peroxide toxicity in Xanthomonas campestris pv. phaseoli (Xp). The expression of both katA and ahpC is controlled by the global peroxide sensor and transcriptional activator, OxyR. In Xp, these two genes have compensatory expression patterns. Inactivation of katA leads to an increase in the level of AhpC and a concomitant increase in resistance to tert-butyl hydroperoxide (tBOOH). High-level expression of katA from an expression vector in Xp also lowered the level of ahpC expression. The compensatory regulation of katA and ahpC was mediated by OxyR, since the compensatory response was not observed in an oxyR mutant background. ahpC and katA play important but unequal roles in protecting Xp from H2O2toxicity. These observations, taken together with a previous observation that an ahpC mutant expresses high levels of KatA and is hyper-resistant to H2O2, suggest the possibility that inactivation of either gene leads to accumulation of intracellular H2O2. This in turn oxidizes reduced OxyR and converts the regulator to the oxidized form that then activates expression of genes in the OxyR regulon. © 2005 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.