Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer reviewed journal
Publication Acceptance Date: 3/30/2008
Publication Date: 7/1/2008
Citation: Glenn, A.E., Zitomer, N.C., Zimeri, A.M., Williams, L.D., Riley, R.T., Proctor, R. 2008. Transformation-mediated complementation of a FUM gene cluster deletion in Fusarium verticillioides restores both fumonisin production and pathogenecity on maize seedlings. Molecular Plant-Microbe Interactions. 21:87-97. Interpretive Summary: The fungus Fusarium verticillioides is of significant concern due to its production of the fumonisin mycotoxins, which cause a number of species-specific animal diseases. Questions of “how” and “why” this fungus produces the fumonisins are of particular interest because knowing such information may provide clues regarding how to eliminate or manage fumonisin contamination of food and feed. One hypothesis of why the fungus produces fumonisins is that they are actually intended to weaken the corn plant so that the fungus can acquire nutrients from the compromised tissues. We present data supporting fumonisin production is necessary for F. verticillioides to cause disease symptoms on the leaves of corn seedlings. Non-producing strains were not able to cause foliar disease symptoms on seedlings yet were still able to colonize the seedlings. We also describe a putative deletion of the fumonisin biosynthetic gene cluster in a collection of strains. Such a deletion of the cluster has not been documented previously. Various experimental results supported the conclusion that fumonisin mycotoxins were phytotoxic to corn seedlings and that fumonisin production was essential for causing leaf lesions and other foliar symptoms associated with corn seedling disease.
Technical Abstract: Fusarium verticillioides strains having diverse genetic backgrounds were used to examine the role of fumonisin mycotoxins in development of maize seedling blight. Wild-type, fumonisin-producing strains caused necrotic lesions, atrophy, and bleaching of leaves and severe stunting or death of maize seedlings. Fumonisin-nonproducing strains caused no foliar disease symptoms and maize seedlings generally appeared similar to uninoculated controls. Genetic analysis of ascospore progeny derived from sexual crosses indicated seedling pathogenicity and fumonisin production cosegregated together as a single locus. The fumonisin-nonproducing phenotype of examined strains resulted from differing mutations of genes within fumonisin biosynthetic gene cluster. PCR and Southern hybridizations failed to detect the FUM1, FUM3, FUM12, and FUM19 genes in nonpathogenic, fumonisin-nonproducing strains derived from banana isolate NRRL 25059, suggesting the nonproduction phenotype resulted from an absence of the gene cluster. Gene deletion mutants (fum1 and fum6) unable to produce fumonisins also did not induce foliar disease symptoms in seedlings, while a fumonisin-producing, complemented fum1 mutant did induce severe symptoms. Thus, data suggested fumonisin was phytotoxic and necessary for development of leaf lesions and other foliar disease symptoms, yet systemic colonization of maize seedlings by F. verticillioides was not necessary or sufficient for disease to occur, which supported involvement of a phytotoxin or other mobile signal in induction of disease. Lastly, seedling disease development was dependent on maize genotype and varied in severity between lines. Together, the data implicated fumonisin-production as a pathogenicity factor for foliar disease of maize seedlings.