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item Proctor, Robert
item Butchko, Robert
item Busman, Mark
item Brown, Daren
item Desjardins, Anne

Submitted to: Aflatoxin Workshop
Publication Type: Abstract Only
Publication Acceptance Date: 10/25/2005
Publication Date: 10/25/2005
Citation: Proctor, R., Butchko, R.A., Plattner, R.D., Busman, M., Brown, D.W., Desjardins, A.E. 2005. Polyketide synthases in fusarium verticillioides: potential targets to control fumonisin contamination in corn [abstract]. Proceedings of the 4th Annual Fungal Genomics, 5th Annual Multi-Crop Fumonisin, and 17th Annual Aflatoxin Elimination Workshops. p. 58.

Interpretive Summary:

Technical Abstract: The fungus Fusarium verticillioides negatively impacts corn production in two ways; it produces the mycotoxins fumonisins and it causes diseases such as ear and stalk rot. Fumonisins can cause a number of animal diseases, including cancer and neural tube defects in laboratory rodents. In humans, consumption of fumonisin-contaminated corn has been correlated epidemiologically with esophageal cancer and neural tube defects. Sorting of individual kernels from F. verticillioides-inoculated corn revealed that fumonisin levels are substantially higher in symptomatic kernels compared to asymptomatic kernels (Desjardins & Plattner, 1998, Plant Dis. 82:953-958). This finding indicates that a reduction in ear rot should reduce fumonisin contamination in corn. Thus, a goal of our research is to identify factors that contribute to the ability of F. verticillioides to cause ear rot because such factors are potential targets for disease control. Production of some polyketide-derived metabolites contributes to the ability of a number of fungi (e.g. Cercospora, Cochliobolus, and Phylosticta) to cause plant disease. Therefore, polyketides may contribute to the ability of F. verticillioides to cause corn ear rot. Polyketide synthases (PKSs) typically catalyze an early step in the biosynthesis of polyketides, and disruption of a PKS gene blocks production of the corresponding polyketide(s). Fifteen PKS genes have been identified in the F. verticillioides genome (Kroken et al. 2003. Proc. Nat. Acad. Sci., USA 100:15670-15675). To determine the role of F. verticillioides-produced polyketides in pathogenesis, we are disrupting each PKS gene. To date, we have disrupted eight of the PKS genes and determined that one (PKS10) is required for production of the mycotoxins fusarins (also shown by Song et al 2004, ChemBioChem 5:1196-1203) and another (PKS3) is required for production of the dark pigment in the walls of the sexual fruiting bodies of F. verticillioides. Pathogenicity tests with all eight PKS mutant strains are in progress. Previous Northern blot analysis indicate the fifteen genes in fumonisin biosynthetic (FUM) gene cluster, including the PKS gene FUM1, exhibit similar patterns of expression. This co-expression of FUM genes was also detected by microarray analysis of over 11,000 F. verticillioides EST sequences. Based on these results, we are using microarray analysis to examine the expression patterns of the F. verticillioides PKS genes and their flanking genes to identify polyketide biosynthetic gene clusters. Preliminary analysis suggests that two PKS genes, PKS4 and PKS10, are part of polyketide biosynthetic gene clusters. The eight contiguous genes on one side of PKS10 exhibit co-expression while the genes on the other side do not. Sequence comparisons indicate that six of the co-expressed genes encode enzymes (e.g. oxidoreductases and a carboxymethly transferase) consistent with the predicted fusarin biosynthetic pathway. The seven contiguous genes adjacent to PKS4 also exhibit co-expression.