Skip to main content
ARS Home » Research » Publications at this Location » Publication #103831


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

Submitted to: Society of Industrial Microbiology Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 8/6/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Fumonisins are mycotoxins produced in maize by the ear rot pathogen Fusarium moniliforme. Consumption of fumonisin contaminated maize causes several animal mycotoxicoses and, in certain regions of China and South Africa, is epidemiologically correlated with human esophageal cancer. We study the genetics of fumonisin biosynthesis in order to identify "weak links" in this process that might be exploited to prevent fumonisin contamination of maize. We used degenerate PCR primers and a cDNA template to identify a polyketide synthase gene (FUM5) that is required for fumonisin biosynthesis in F. moniliforme. The predicted amino acid sequence of FUM5 includes regions resembling the enzymatic domains found in other polyketide synthases and its inactivation reduces fumonisin production more than 99%. Sequence analysis of DNA flanking the PKS gene revealed the presence of other open reading frames (ORFs). Classical genetic evidence indicates that fumonisin biosynthetic genes are tightly linked. Thus, FUM5 and the flanking ORFs may be part of a fumonisin biosynthetic gene cluster. The identification of fumonisin biosynthetic genes will allow us to generate fumonisin-nonproducing mutants of F. moniliforme. These mutants may be useful in biological control of ear rot and in determining whether fumonisins are required for virulence of the fungus.