|KIM, WONYONG - Washington State University
|PEEVER, TOBIN - Washington State University
Submitted to: Food Legume Research International Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 6/30/2014
Publication Date: 7/1/2014
Citation: Kim, W., Peever, T., Vandemark, G.J., Chen, W. 2014. What roles do fungal secondary metabolites play in interactions between Ascochyta fungi and cool season food legumes [abstract]? Food Legume Research International Conference Proceedings. Conference Abstract Book.
Technical Abstract: Fungal plant pathogens produce many secondary metabolites including many that are toxic to plants (phytotoxins). Some of these phytotoxins are host-selective (toxic only to particular genotypes of host plants) and required for pathogenicity, while many others are non host-selective and toxic to many different plants. The Ascochyta blight pathogens of cool season food legumes produce an array of non host-selective toxins. Although Ascochyta blight pathogens are generally host-specific, their phytotoxins are not. Nevertheless, these phytotoxins have often been proposed to be virulence/pathogenicity factors without conclusive evidence. We are currently investigating the roles of secondary metabolites produced by the Ascochyta blight pathogens in their pathogenicity and ecology. We found that each Ascochyta species produces a unique set of secondary metabolites, which is highly correlated to evolutionary relationships inferred among the species. For the chickpea blight pathogen, all isolates of Ascochyta rabiei produce solanapyrone toxins, which are unique among Ascochyta species, but identical to those produced by the potato pathogen, Alternaria solani. During studying the roles of solanopyrones in pathogenesis, the solanapyrone synthase gene in both Ascochyta rabiei and Alternaria solani was disrupted through targeted gene replacement. The resulting mutants do not produce solanapyrones, but accumulate the precursor presolanopyrone which is not toxic to plants. Surprisingly, these solanapyrone-deficient mutants are equally pathogenic, if not more pathogenic, than the wild-type strains, on their respective hosts. Results show that the solanapyrone toxins are not required for pathogenicity, but may play important roles in the biology of these fungi including competition and survival in nature.