The major Cu,Zn SOD of the phytopathogen Claviceps purpurea is not essential for pathogenicity.

summary Superoxide dismutase (SOD) activities of the biotrophic pathogen Claviceps purpurea, which causes the ergot disease on a wide range of host grasses, were examined in axenic and pathogenic cultures. Almost all SOD activity in axenic culture originated from a single Cu,Zn SOD; a substantial part of this activity could be separated from lyophilized intact mycelia by gentle washing, indicating that this protein is at least partially secreted. The corresponding gene (cpsod1) was cloned and characterized; like other fungal Cu,Zn SOD genes, it groups with the extracellular mammalian Cu,Zn SODs in a phylogenetic tree. Northern analyses showed that cpsod1 is strongly induced by copper and weakly induced by iron; superoxide generated by paraquat, or xanthine and xanthine oxidase, as well as hydrogen peroxide, had no effect on gene expression under axenic conditions. Analysis of the deletion mutant Deltacpsod1 showed that, although growth in axenic culture was generally slower, sensitivity to paraquat was not increased in comparison to the wild-type. Pathogenicity assays showed that this gene is not essential for parasitic growth in rye; no further soluble SOD activity is induced in the mutant.