Skip to main content
ARS Home » Research » Publications at this Location » Publication #96312


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

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 10/31/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Fumonisins are polyketide mycotoxins produced by Gibberella fujikuroi mating population A (Fusarium moniliforme), a major pathogen of maize worldwide. The high incidence of fumonisin contamination in maize and the phytotoxicity of fumonisins indicate that fumonisins may play a role in pathogenesis on maize. Meiotic analysis has identified closely linked fumonisin biosynthetic loci, fum1, fum2, and fum3. Strains with the fum1- mutation produce no fumonisins, whereas strains with fum2- and fum3- mutations accumulate fumonisins B2 and B3, respectively, instead of fumonisin B1. To test the role of fumonisins in pathogenesis on maize under field conditions, fum1-, fum2-, and fum3- mutants were injected into the silk channel of maize ears. All three mutants retained wild-type ability to cause ear rot. The fum1- mutant produced no fumonisins in the rotted ears. These results contradict a major role for fumonisins in maize ear rot but require confirmation by targeted disruption of fumonisin biosynthesis genes. We have recently identified a cosmid that carries a polyketide synthase (PKS) gene with the predicted enzymatic domains, including ketosynthase, acyltransferase, dehydratase, and enoyl reductase. Transformation of the fum1- mutant with this cosmid restored wild-type fumonisin production. Targeted disruption of the PKS gene abolished fumonisin production, indicating that this PKS is essential for fumonisin biosynthesis. Fumonisin nonproducing mutants obtained by PKS gene disruption will be critical tools to rigorously test the role of fumonisins in pathogenesis on maize and other plants.