Publication: Exposure to cadmium elevates expression of genes in the OxyR and OhrR regulons and induces cross-resistance to peroxide killing treatment in Xanthomonas campestris
2
Issued Date
2005-04-01
Resource Type
ISSN
00992240
Other identifier(s)
2-s2.0-17444408182
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Applied and Environmental Microbiology. Vol.71, No.4 (2005), 1843-1849
Suggested Citation
Peerakan Banjerdkij, Paiboon Vattanaviboon, Skorn Mongkolsuk Exposure to cadmium elevates expression of genes in the OxyR and OhrR regulons and induces cross-resistance to peroxide killing treatment in Xanthomonas campestris. Applied and Environmental Microbiology. Vol.71, No.4 (2005), 1843-1849. doi:10.1128/AEM.71.4.1843-1849.2005 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/16365
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Exposure to cadmium elevates expression of genes in the OxyR and OhrR regulons and induces cross-resistance to peroxide killing treatment in Xanthomonas campestris
Other Contributor(s)
Abstract
Cadmium is an important heavy metal pollutant. For this study, we investigated the effects of cadmium exposure on the oxidative stress responses of Xanthomonas campestris, a soil and plant pathogenic bacterium. The exposure of X. campestris to low concentrations of cadmium induces cross-protection against subsequent killing treatments with either H2O2 or the organic hydroperoxide tert-butyl hydroperoxide (tBOOH), but not against the superoxide generator menadione. The cadmium-induced resistance to peroxides is due to the metal's ability to induce increased levels of peroxide stress protective enzymes such as alkyl hydroperoxide reductase (AhpC), monofunctional catalase (KatA), and organic hydroperoxide resistance protein (Ohr). Cadmium-induced resistance to H2O2 is dependent on functional OxyR, a peroxide-sensing transcription regulator. Cadmium-induced resistance to tBOOH shows a more complex regulatory pattern. The inactivation of the two major sensor-regulators of organic hydroperoxide, OxyR and OhrR, only partially inhibited cadmium-induced protection against tBOOH, suggesting that these genes do have some role in the process. However, other, as yet unknown mechanisms are involved in inducible organic hydroperoxide protection. Furthermore, we show that the cadmium-induced peroxide stress response is mediated by the metal's ability to predominately cause an increase in intracellular concentrations of organic hydroperoxide and, in part, H 2O2. Analyses of various mutants of peroxide-metabolizing enzymes suggested that this increase in organic hydroperoxide levels is, at least in part, responsible for cadmium toxicity in Xanthomonas. Copyright © 2005, American Society for Microbiology. All Rights Reserved.