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item Proctor, Robert
item Desjardins, Anne
item Plattner, Ronald
item Brown, Daren

Submitted to: Aflatoxin Workshop
Publication Type: Abstract Only
Publication Acceptance Date: 10/26/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Fusarium verticillioides causes a maize ear rot and produces fumonisins, a family of polyketide-derived mycotoxins. Fumonisins have been implicated as the cause of several animals' diseases, including cancer in rodents, leukoencaphalomalacia in horses and pulmonary edema in swine. There is also an epidemiological correlation between the consumption of fumonisin-contaminated maize and human esophageal cancer in some areas of the world. We are examining the genetics and biochemistry of fumonisin biosynthesis to identify processes that can be exploited to control fumonisin contamination in maize. Early classical genetic studies revealed 3 tightly linked loci, Fum1, Fum2, and Fum3, that confer qualitative differences in fumonisin production in F. verticillioides. More recently, we identified a polyketide synthase gene (FUM5) that is required for fumonisin production. Sequence analysis of the 75-kb region on either side FUM5 revealed the presence of 22 additional genes. Northern analysis has revealed that the 14 genes immediately downstream of FUM5 are coregulated and that their expression is correlated with fumonisin production. In contrast, the expression of three genes further downstream and five genes upstream of FUM5 is not correlated with fumonisin production. Disruption analyses to determine whether the coregulated genes are required for fumonisin biosynthesis are in progress. To date, we have found that two genes are required for fumonisin biosynthesis while three others are not. The predicted translation products of most of the 14 co-regulated genes share similarity with the types of enzymes that are expect to be required for the synthesis of fumonisins.