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

Authors

  • Nisanart Charoenlap,

    1. Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand
    Search for more papers by this author
  • Warawan Eiamphungporn,

    1. Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand
    Search for more papers by this author
  • Nopmanee Chauvatcharin,

    1. Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand
    Search for more papers by this author
    • 1

      Center for Vectors and Vector-Borne Diseases, Mahidol University, Bangkok 10400, Thailand.

  • Supa Utamapongchai,

    1. Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand
    Search for more papers by this author
  • Paiboon Vattanaviboon,

    Corresponding author
    1. Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand
      *Corresponding author. Tel.: +662 574 0623x3815; fax: +662 574 2027., E-mail address: paiboon@tubtim.cri.or.th
    Search for more papers by this author
  • Skorn Mongkolsuk

    1. Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand
    2. Department of Biotechnology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand
    Search for more papers by this author

  • Edited by C.W. Penn

*Corresponding author. Tel.: +662 574 0623x3815; fax: +662 574 2027., E-mail address: paiboon@tubtim.cri.or.th

Abstract

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 H2O2 toxicity. 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.

Ancillary