Karnjana HrimpengBenjaphorn PrapagdeePeerakan BanjerdkijPaiboon VattanaviboonJames M. DubbsSkorn MongkolsukChulabhorn Research InstituteAsian Institute of Technology ThailandMahidol University2018-08-202018-08-202006-09-01FEMS Microbiology Letters. Vol.262, No.1 (2006), 121-12715746968037810972-s2.0-33747045520https://repository.li.mahidol.ac.th/handle/123456789/22987Xanthomonas encounters highly toxic reactive oxygen species (ROS) from many sources, such as those generated by plants against invading bacteria, other soil bacteria and from aerobic respiration. Thus, conditions that alter intracellular ROS levels such as exposure to toxic metalloids would have profound effects on bacterial physiology. Here, we report that exposure of Xanthomonas campestris pv. phaseoli (Xp) to low levels of arsenic induces physiological cross-protection against killing by H2O2 and organic hydroperoxide but not a superoxide generator. Cross-protection against H2O2 and organic hydroperoxide toxicity was due to increased expression of genes encoding major peroxide-metabolizing enzymes such as alkyl hydroperoxide reductase (AhpC), catalase (KatA) and organic hydroperoxide resistance protein (Ohr). Arsenic-induced protection against H2O2 and organic hydroperoxide requires the peroxide stress response regulators, OxyR and OhrR, respectively. Moreover, analyses of double mutants of the major H2O2 and organic hyproperoxide-scavenging enzymes, Xp ahpC katA and Xp ahpC ohr, respectively, suggested the existence of unidentified OxyR- and OhrR-regulated genes that are involved in arsenic-induced resistance to H2O2 and organic hyproperoxide killing in Xp. These arsenic-induced physiological alterations could play an important role in bacterial survival both in the soil environment and during plant-pathogen interactions. © 2006 Federation of European Microbiological Societies Published by Blackwell Publishing Ltd. All rights reserved.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyImmunology and MicrobiologyArticleSCOPUS10.1111/j.1574-6968.2006.00383.x