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Title: ANALYSIS OF A GIBBERELLA FUJIKUROI MUTANT DEFICIENT IN A HYDROXYLATION STEP OF FUMONISIN BIOSYNTHESIS

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

Submitted to: Fungal Genetics Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 3/23/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Gibberella fujikuroi mating population A is a pathogen of maize and sorghum and produces a family of toxins known as fumonisins that are associated with a number of mycotoxicoses. The B-type fumonisins consist of a 20-carbon-long backbone with two tricarboxylic acid moieties and one amino, two methyl, one to three hydroxyl groups. We have employed UV mutagenesis to study the genetics of fumonisin biosynthesis in G. fujikuroi. Three hundred forty-three strains derived from conidia that survived UV exposure were analyzed for their ability to produce fumonisins. Nine of the survivors failed to produce fumonisins and one (uv26) only produced fumonisin B3, which lacks the hydroxyl group at carbon atom 5 (C-5). Wild-type strains of the fungus produce fumonisins B1 and B2, which are C-5 hydroxylated, as well as B3. Genetic analyses revealed that the mutation segregates as a single locus and is linked to the fum2 and fum3 loci (previously identified in natural variants), the RAPD marker OPA16, and a putative aldehyde dehydrogenase gene on chromosome 1 of G. fujikuroi. In addition, fum3- and the uv26 mutation may be allelic because both confer the same fumonisin phenotype and no recombinant progeny were recovered from a cross between strains carrying these two markers. Currently, we are attempting to complement the uv26 mutation by transformation with cosmid libraries constructed with DNA from wild-type strains of G. fujikuroi.