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item Proctor, Robert
item Plattner, Ronald
item Desjardins, Anne
item Busman, Mark
item Butchko, Robert

Submitted to: Journal of Agricultural and Food Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/17/2006
Publication Date: 3/22/2006
Citation: Proctor, R.H., Plattner, R.D., Desjardins, A.E., Busman, M., Butchko, R.A.E. 2006. Fumonisin production in the corn pathogen Fusarium verticillioides: the genetic basis of naturally occurring chemical variation. Journal of Agricultural and Food Chemisty. 54:2424-2430.

Interpretive Summary: Ear and stalk rot, a common disease on maize, is caused by a fungus called Fusarium verticillioides. In addition to causing rot on maize ears, this fungus also produces toxic chemicals, or mycotoxins, called fumonisins. We are interested in understanding the biology and genetics of fumonisin production by F. verticillioides in order to try to reduce or eliminate these mycotoxins in maize. In this report, we describe the role of two genes involved in the production of fumonisins. We have used molecular genetic experiments to study the functions of these genes. This approach has allowed us to more fully understand the process of fumonisin production. A better understanding of the genes involved in fumonisin production may lead to novel strategies for controlling mycotoxin contamination of maize.

Technical Abstract: Fumonisins are polyketide-derived mycotoxins produced by the maize pathogen Fusarium verticillioides. Previous analyses identified naturally occurring variants of the fungus that are deficient in fumonisin C-10 hydroxylation or that do not produce any fumonisins. In the current study, gene deletion and genetic complementation analyses localized the C-10 hydroxylation deficiency to a cytochrome P450 monooxygenase gene in the fumonisin biosynthetic gene (FUM) cluster. Sequence analysis indicated that the hydroxylation deficiency resulted from a single nucleotide insertion that caused a frame shift in the protein coding region. Genetic complementation localized the fumonisin-nonproduction phenotype to the polyketide synthase gene in the FUM cluster, and sequence analysis indicated that the nonproduction phenotype resulted from a nucleotide substitution, which introduced a premature stop codon in the coding region. These results provide the first direct evidence that altered fumonisin production phenotypes of naturally occurring F. verticillioides variants can result from single point mutations in the FUM cluster.