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United States Department of Agriculture

Agricultural Research Service

Title: Genetic Complementation and Virulence of a Fumonisin Nonproducing Mutant (Fum1) of Gibberella Fujikuroi Mating Population A

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

Submitted to: American Phytopathological Society Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: November 12, 1998
Publication Date: N/A

Technical Abstract: Fumonisins are polyketide toxins produced by Gibberella fujikuroi mating population A (Fusarium moniliforme), a major pathogen of maize worldwide. Fumonisins are sphingolipid-analogue mycotoxins that can cause equine leucoencephalomalacia, porcine pulmonary edema, and liver cancer in rats. Meiotic analysis has identified a number of closely linked fumonisin biosynthetic loci including fum1, a mutant of which does not produce any detectable fumonisins. We have recently identified a cosmid that carries a polyketide synthase gene with enzymatic domains for ketosynthase, acyltransferase, dehydratase, enoyl reductase, and ketoreductase. Transformation of the fum1 mutant with this cosmid restored wild-type fumonisin production. This cosmid carries at least two other genes and is being subcloned to localize fum1 and to determine the role of all of the genes in fumonisin biosynthesis. Because fumonisins are phytotoxic they have been hypothesized to play a role in pathogenesis on maize. To test this hypothesis under field conditions, a fum1- mutant was injected into the silk channel of maize ears at silking. The fum1- mutant retained wild-type ability to cause maize ear rot but did not produce any detectable fumonisins in the ears. These preliminary results contradict a major role for fumonisins in maize ear rot but should be confirmed by targeted gene disruption. The recent isolation of the polyketide synthase and other putative fumonisin biosynthetic genes will make this approach possible.

Last Modified: 4/17/2015
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