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ARS Home » Research » Publications at this Location » Publication #109902
Title: BIOSYNTHETIC AND GENETIC RELATIONSHIPS OF B-SERIES FUMONISINS PRODUCED BY GIBBERELLA FUJIKUROI MATING POPULATION A

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

Submitted to: Natural Toxins
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/23/2000
Publication Date: N/A
Citation: N/A

Interpretive Summary: The fungus Gibberella fujikuroi causes ear and root rot of corn. The fungus also produces a group of carcinogenic toxins, known as fumonisins, in infected corn. These toxins cause a number of diseases is animals, including a fatal lung disease (edema) in swine and a fatal brain disease (leucoencephalomalcia) in horses. There is also a correlation between the consumption of corn contaminated with fumonisins and human esophageal cancer in some areas of the world where corn is a dietary staple. In this study, we determined the order of three genetic loci that are involved in fumonisin biosynthesis along chromosome 1 of G. fujikuroi. In addition, we found that the fumonisin biosynthesis branches into two pathways. One branch leads to the formation of fumonisin B1 and the other leads to the formation of fumonisin B2. These findings provide further insight into how fumonisins are produced and may eventually reveal weak links that can be exploited to control fumonisin contamination in corn.

Technical Abstract: Fumonisins are mycotoxins produced by the maize pathogen Gibberella fujikuroi mating population A (MP-A) and are frequently present in maize kernels. Wild-type strains of the fungus produce four B-series fumonisins, FB1, FB2, FB3, and FB4. These four toxins are identical in structure except for the number and positions of hydroxyl groups along their linear carbon backbone. To elucidate the genetic and biosynthetic relationship among these fumonisins, we conducted meiotic and biochemical analyses of G. fujikuroi MP-A mutants with altered fumonisin production phenotypes that result from defective alleles at three fumonisin biosynthetic loci, Fum1, Fum2, and Fum3. These mutants produced either no fumonisins, only FB2 and FB4, or only FB3 and FB4. Genetic analyses revealed the orientation of the three Fum loci along linkage group 1 of the fungus. The mutants were also grown together in pair-wise combinations to determine if their fumonisin production phenotypes could be complemented. When FB3-producing mutants were grown with FB2-producing mutants, complementation occurred. However, when a nonproducing mutant was grown with either a F2- or FB3-producing mutant, complementation either did not occur or was incomplete. When purified FB2, FB3, or FB4 was fed to mutant cultures, FB4 was converted primarily to FB2, FB3 was converted to FB1, and FB2 was not converted. The results from the complementation and feeding assays suggest a previously unrecognized branch in the fumonisin biosynthetic pathway in G. fujikuroi MP-A.