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

• Published in: FEMS microbiology letters 2005-08, Vol.249 (1), p.73-78
• Main Authors: Charoenlap, Nisanart, Eiamphungporn, Warawan, Chauvatcharin, Nopmanee, Utamapongchai, Supa, Vattanaviboon, Paiboon, Mongkolsuk, Skorn
• Format: Article
• Language: English
• Subjects: ahpC; Alkyl hydroperoxide reductase; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacteriology; Biological and medical sciences; Butyl hydroperoxide; Catalase; Catalase - genetics; Catalase - metabolism; Deactivation; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation, Bacterial; Genes; Genetics; H 2O 2; H2O2; Heat-Shock Response; Hydrogen peroxide; Hydrogen Peroxide - pharmacology; Inactivation; katA; Microbiology; Oxidative Stress; OxyR; Peroxidases - genetics; Peroxidases - metabolism; Peroxiredoxins; Reductases; Repressor Proteins - genetics; Repressor Proteins - metabolism; Toxicity; Transcription; Transcription Factors - genetics; Transcription Factors - metabolism; Xanthomonas; Xanthomonas campestris; Xanthomonas campestris - enzymology; Xanthomonas campestris - genetics; Xanthomonas campestris - physiology
• ISSN: 0378-1097; 1574-6968
• DOI: 10.1016/j.femsle.2005.06.002

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 H 2O 2 toxicity. These observations, taken together with a previous observation that an ahpC mutant expresses high levels of KatA and is hyper-resistant to H 2O 2, suggest the possibility that inactivation of either gene leads to accumulation of intracellular H 2O 2. This in turn oxidizes reduced OxyR and converts the regulator to the oxidized form that then activates expression of genes in the OxyR regulon.