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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Veröffentlicht in:FEMS microbiology letters 2005-08, Vol.249 (1), p.73-78
Hauptverfasser: Charoenlap, Nisanart, Eiamphungporn, Warawan, Chauvatcharin, Nopmanee, Utamapongchai, Supa, Vattanaviboon, Paiboon, Mongkolsuk, Skorn
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container_issue 1
container_start_page 73
container_title FEMS microbiology letters
container_volume 249
creator Charoenlap, Nisanart
Eiamphungporn, Warawan
Chauvatcharin, Nopmanee
Utamapongchai, Supa
Vattanaviboon, Paiboon
Mongkolsuk, Skorn
description 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.
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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.</description><subject>ahpC</subject><subject>Alkyl hydroperoxide reductase</subject><subject>Bacterial Proteins - genetics</subject><subject>Bacterial Proteins - metabolism</subject><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>Butyl hydroperoxide</subject><subject>Catalase</subject><subject>Catalase - genetics</subject><subject>Catalase - metabolism</subject><subject>Deactivation</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Fundamental and applied biological sciences. 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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. 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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
title OxyR mediated compensatory expression between ahpC and katA and the significance of ahpC in protection from hydrogen peroxide in Xanthomonas campestris
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