title: Challenging Xanthomonas campestris with low levels of arsenic mediates cross-protection against oxidant killing.
abstract: Xanthomonas 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 H(2)O(2) and organic hydroperoxide but not a superoxide generator. Cross-protection against H(2)O(2) 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 H(2)O(2) and organic hydroperoxide requires the peroxide stress response regulators, OxyR and OhrR, respectively. Moreover, analyses of double mutants of the major H(2)O(2) 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 H(2)O(2) 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.
authors.affiliation: Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok, Thailand.
authors.forename: Karnjana
authors.initials: K
authors.lastname: Hrimpeng
authors.forename: Benjaphorn
authors.initials: B
authors.lastname: Prapagdee
authors.forename: Peerakan
authors.initials: P
authors.lastname: Banjerdkij
authors.forename: Paiboon
authors.initials: P
authors.lastname: Vattanaviboon
authors.forename: James M
authors.initials: JM
authors.lastname: Dubbs
authors.forename: Skorn
authors.initials: S
authors.lastname: Mongkolsuk
mesh_terms: D000222:Adaptation, Physiological; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D018053:Arsenites / Q000378:metabolism / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000096:biosynthesis; D015152:Blotting, Northern; D002374:Catalase / Q000096:biosynthesis; D015169:Colony Count, Microbial; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D005809:Genes, Regulator; D006861:Hydrogen Peroxide / Q000494:pharmacology; D016877:Oxidants / Q000494:pharmacology*; D010544:Peroxidases / Q000096:biosynthesis; D054464:Peroxiredoxins; D017670:Sodium Compounds / Q000378:metabolism / Q000494:pharmacology*; D016959:Xanthomonas campestris / Q000187:drug effects* / Q000235:genetics / Q000502:physiology*
chemical_list: D000900:Anti-Bacterial Agents; D018053:Arsenites; D001426:Bacterial Proteins; D016877:Oxidants; D017670:Sodium Compounds; C112257:organic hydroperoxide resistance protein, Xanthomonas campestris; C017947:sodium arsenite; D006861:Hydrogen Peroxide; D010544:Peroxidases; D054464:Peroxiredoxins; D002374:Catalase