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Title: Functional analyses of the Diels-Alderase gene sol5 of Ascochyta rabiei and Alternaria solani indicate that the Solanapyrone phytotoxins are not required for pathogenicity

Author
item KIM, WONYONG - Washington State University
item PARK, CHUNG-MIN - Washington State University
item PARK, JEONG-JIN - Washington State University
item AKAMATSU, HAJIME - National Agricultural Research Center - Japan
item PEEVER, TOBIN - Washington State University
item XIAN, MING - Washington State University
item GANG, DAVID - Washington State University
item Vandemark, George
item Chen, Weidong

Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/24/2014
Publication Date: 4/1/2015
Citation: Kim, W., Park, C., Park, J., Akamatsu, H.O., Peever, T., Xian, M., Gang, D.R., Vandemark, G.J., Chen, W. 2015. Functional analyses of the Diels-Alderase gene sol5 of Ascochyta rabiei and Alternaria solani indicate that the Solanapyrone phytotoxins are not required for pathogenicity. Molecular Plant-Microbe Interactions. 28:482-496.

Interpretive Summary: The devastating chickpea fungal pathogen Ascochyta rabiei is known to produce the same solanapyrone toxins as the potato pathogen Alternaria solani does, and the toxins have long been suspected to play important roles in causing disease without rigorous proof. Using targeted gene replacement technology, we generated mutants of both pathogens that completely lost ability to produce the toxins. Surprisingly the toxin-minus mutants are just as virulent as their parental strains on their respective host plants, providing strong evidence that the solanapyrone toxins are not required for pathogenicity. Exonerating solanapyrone toxins as pathogenicity factors will stimulate research to search for real pathogenicity determinants for a better understanding of pathogenesis and novel strategies to develop resistant cultivars and more efficient practices for managing the diseases.

Technical Abstract: Ascochyta rabiei and Alternaria solani, the causal agents of Ascochyta blight of chickpea (Cicer arietinum) and early blight of potato (Solanum tuberosum), respectively, produce a set of phytotoxic compounds incuding solanapyrones A, B, and C. Although both the phytotoxicity of solanopyrones and their universal production among field isolates have been documented, the role of solanapyrones in pathogenicity is not well understood. Here we report the functional characterization of the sol5 gene, which encodes a Diels-Alderase that catalyzes the final step of solanapyrone biosynthesis. Deletion of sol5 in both A. rabiei and Al. solani completely prevented production of solanapyrones and led to accumulation of the immediate precursor compound prosolanapyrone II-diol, which is not toxic to plant. Deletion of sol5 led to overexpression of the other solanapyrone biosynthesis genes, suggesting a possible feedback regulation mechanism. The mutants showed growth rates and spore production similar to the wild-type progenitors in vitro. Phytotoxicity tests showed that solanapyrone A is highly toxic to several legume species and Arabidopsis thaliana. Despite the apparent phytotoxicity of solanapyrone A, pathogenicity tests showed that solanapyrone-minus mutants of A. rabiei and Al. solani were equally pathogenic as their corresponding wild-type progenitors, suggesting that solanapyrones are not required for pathogenicity.