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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 #199026


item Proctor, Robert
item Butchko, Robert
item Brown, Daren
item Busman, Mark
item Plattner, Ronald

Submitted to: Corn Dry Milling Conference
Publication Type: Abstract Only
Publication Acceptance Date: 6/1/2006
Publication Date: 6/1/2006
Citation: Proctor, R., Butchko, R.A., Brown, D.W., Busman, M., Plattner, R.D. 2006. Fusarium genomics as a tool to control mycotoxins [abstract]. 47th Annual Corn Dry Milling Conference. p. 5.

Interpretive Summary:

Technical Abstract: The fungus Fusarium verticillioides can cause ear and stalk rot of corn and can produce the carcinogenic mycotoxins, fumonisins, in infected corn kernels. One long term goal of the Mycotoxin Research Unit at NCAUR is to eliminate or reduce fumonisins in U.S. corn. To address this goal, we are conducting a genomic analysis of F. verticillioides. That is, we are identifying and examining the expression of thousands of genes in the fungus in an attempt to identify targets that can be exploited to control fumonisin production and/or ear rot. In collaboration with researchers at The Institute for Genomic Research, we have developed two genomic tools, an expressed sequence tag (EST) library and DNA chips. The EST library is a database containing partial sequences of ~11,000 F. verticillioides genes. The DNA chips, or microarrays, consist of short pieces of all ~11,000 sequences affixed to a glass microscope slide. The DNA chips are being used to examine expression of all ~11,000 F. verticillioides genes simultaneously. One area of focus is polyketide synthase genes as potential targets to control fumonisins and/or corn ear rot. These genes encode enzymes that catalyze the first step in the biosynthesis of polyketide secondary metabolites. In other fungal species, production of polyketides can contribute to the ability to cause plant disease. For example, production of the polyketide T toxin increases the severity of southern corn leaf blight caused by the fungus Cochliobolus heterostrophus, and production of the polyketide cercosporin increases the severity of leaf and stem diseases caused by Cercospora. Thus, it is possible that production of one or more polyketides by F. verticillioides increases the severity of corn ear rot and thereby its ability to produce fumonisins in corn. A previous genomic sequence analysis identified 15 polyketide synthase (PKS) genes in F. verticillioides, and partial sequences of most of these genes are present in our EST library. We are characterizing these genes to determine: (1) the polyketide metabolites synthesized by the PKSs; (2) whether production of the polyketide metabolites contributes to pathogenesis on corn; and (3) whether the PKS genes are located within gene clusters. Gene inactivation experiments of eight of the PKS genes indicate that one of the genes (PKS3) is required for production of the dark fruiting body pigment, that another (PKS4) is required for production of the pigment bikaverin, and a third gene (PKS10) is required for production of the toxins, fusarins, as reported in other Fusarium species. Microarray analysis indicated that PKS10 and PKS4 are located within clusters of genes that are co-expressed. In addition, we are currently conducting field tests to determine if inactivation of any of the polyketide synthase genes affects the ability of F. verticillioides to cause corn ear rot.