Protection of Xanthomonas against arsenic toxicity involves the peroxide-sensing transcription regulator OxyR.

Arsenic has been shown to mediate its toxicity through induced generation of reactive oxygen species. Here, we examined the role of oxidative stress-inducible genes (katA, ahpC and ohr) and their regulators (oxyR and ohrR) in the response to arsenic treatment in a plant pathogenic bacterium, Xanthomonas campestris pv. phaseoli (Xp). Overproduction of peroxide-scavenging enzymes (KatA, AhpCF and Ohr) did not enhance arsenic tolerance in wild-type Xp. Furthermore, inactivation of katA, ahpC, ohr, and ohrR genes had no effect on the level of arsenic resistance. By contrast, an oxyR mutant (Xp oxyR) showed increased sensitivity to both pentavalent arsenate and, to a greater extent, trivalent arsenite. The resistance of cells to arsenite treatment was significantly affected by the level of iron. Cells were 10-fold more sensitive to arsenite killing in the presence of excess iron, while removal of iron by an iron chelator (2,2'-dipyridyl) protected Xanthomonas from arsenite toxicity. The arsenite-sensitive phenotype of Xp oxyR could be complemented by the expression of functional OxyR from a plasmid vector, but not by the expression of other known OxyR-regulated peroxide-scavenging enzymes such as KatA and AhpCF, Ohr and OhrR. The data suggested that as yet unidentified, OxyR-regulated gene(s) are involved in conferring arsenic resistance in Xp. To our knowledge, this is the first report showing that the peroxide-sensing regulator OxyR is involved in arsenic resistance.