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ARS Home » Midwest Area » Peoria, Illinois » National Center for Agricultural Utilization Research » Mycotoxin Prevention and Applied Microbiology Research » Research » Publications at this Location » Publication #213988
Title: Complementary host-pathogen genetic analyses of the role of fumonisins in the Zea mays-Gibberella moniliformis seedling interaction

Author
item Desjardins, Anne
item Busman, Mark
item Muhitch, Michael
item Proctor, Robert

Submitted to: Physiological and Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/5/2007
Publication Date: 11/20/2007
Citation: Desjardins, A.E., Busman, M., Muhitch, M.J., Proctor, R. 2007. Complementary host-pathogen genetic analyses of the role of fumonisins in the Zea mays-Gibberella moniliformis seedling interaction. Physiological and Molecular Plant Pathology. 70(4-6):149-160.

Interpretive Summary: The fungus Gibberella moniliformis causes maize (corn) seedling blight and ear rot, and contaminates grain with fumonisin toxins that are harmful to health. In this study we developed lines of maize that are insensitive to these toxins and showed that these lines of maize are still susceptible to seedling blight. This research should be of interest to maize pathologists and breeders by providing new information on the importance of fumonisins in maize diseases.

Technical Abstract: Zea mays often is colonized with the fungus Gibberella moniliformis, which produces fumonisin toxins. The role of fumonisins in seedling colonization and blight was studied using complementary genetic analyses of host and pathogen. Only two of four fumonisin B1 (FB1)-insensitive maize backcross lines were more resistant than the FB1-sensitive parent to seedling blight, indicating that the increase in FB1-insensitivity was not associated with an increase in resistance. FB1-producing and nonproducing isogenic fungal strains did not differ in ability to cause seedling blight, but the FB1-producing strain was more effective in systemic colonization of seedlings in reciprocal strain challenge tests. Together, these and previous results indicate that the role of fumonisins depends on complex environmental and genetic contexts in this host-pathogen interaction.