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Applied and Environmental Microbiology, April 2005, p. 1843-1849, Vol. 71, No. 4
0099-2240/05/$08.00+0     doi:10.1128/AEM.71.4.1843-1849.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Exposure to Cadmium Elevates Expression of Genes in the OxyR and OhrR Regulons and Induces Cross-Resistance to Peroxide Killing Treatment in Xanthomonas campestris

Peerakan Banjerdkij,1,2 Paiboon Vattanaviboon,1* and Skorn Mongkolsuk1,3*

Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si,1 Postgraduate Education, Training and Research Program in Environmental Science, Technology and Management, Asian Institute of Technology,2 Department of Biotechnology, Faculty of Science, Mahidol University, Bangkok, Thailand3

Received 30 July 2004/ Accepted 22 October 2004

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, H2O2. 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.

* Corresponding author. Mailing address: Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand. Phone: (662) 574-0630, ext. 3816. Fax: (662) 574-2027. E-mail for Paiboon Vattanaviboon: paiboon{at}tubtim.cri.or.th. E-mail for Skorn Mongkolsuk: skorn{at}tubtim.cri.or.th.

* Corresponding author. Mailing address: Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand. Phone: (662) 574-0630, ext. 3816. Fax: (662) 574-2027. E-mail for Paiboon Vattanaviboon: paiboon{at}tubtim.cri.or.th. E-mail for Skorn Mongkolsuk: skorn{at}tubtim.cri.or.th.

Applied and Environmental Microbiology, April 2005, p. 1843-1849, Vol. 71, No. 4
0099-2240/05/$08.00+0     doi:10.1128/AEM.71.4.1843-1849.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Helbig, K., Grosse, C., Nies, D. H. (2008). Cadmium Toxicity in Glutathione Mutants of Escherichia coli. J. Bacteriol. 190: 5439-5454 [Abstract] [Full Text]  


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