Transcriptional regulation by iron and role during plant pathogenesis of genes encoding iron- and manganese-superoxide dismutases of Pseudomonas syringae pv. syringae B728a

Abstract

The bean pathogen, Pseudomonas syringae B728a, may require iron-superoxide dismutase (FeSOD) and manganese–superoxide dismutase (MnSOD) activities in protection against reactive oxygen species (ROS) generated in planta. Genes encoding FeSOD or MnSOD of P. syringae B728a were cloned by hybridization with specific PCR probes amplified from P. syringae genomic DNA. The sodB gene was monocistronic whereas the sodA gene was transcribed as part of a 1.4 kb polycistronic operon, consisting of orfX-sodA. A putative Fur consensus sequence was located upstream of the orfX-sodA operon. The sodB (FeSOD) gene was expressed throughout growth, but was down regulated under iron deficient conditions. In contrast, the sodA (MnSOD) gene was expressed only under iron deficient conditions. Mutants defective in sodA and sodB genes were generated by marker exchange mutagenesis. Unlike other bacterial SOD deficient mutants, the P. syringae B728a sodAsodB mutant was not impaired in growth on rich or minimal medium, but it was more sensitive to paraquat than wild-type. The P. syringae B728a SOD deficient mutants caused bacterial brown spot disease on bean pods or leaves to the same extent as wild-type. Thus, these superoxide dismutases may not be key enzymes for aerobic metabolism and pathogenicity in P. syringae B728a.