Submitted to: Gordon Research Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: March 23, 2003
Publication Date: N/A
Technical Abstract: Gibberella moniliformis causes ear and stalk rot of maize and can produce the polyketide-derived mycotoxins fumonisin B1, B2, B3 and B4. Fumonisins disrupt sphingolipid biosynthesis in animal cells, cause leukoencephalomalacia and pulmonary edema in horses and swine respectively, and are associated with liver and kidney cancer in laboratory rodents. A fumonisin biosynthetic gene (FUM) cluster, consisting of 15 co-regulated genes, was recently described in G. moniliformis. BLAST comparisons indicate that most genes in the cluster are likely to encode proteins involved in fumonisin biosynthetic reactions. During our ongoing deletion analysis of FUM genes, we have been able to determine the molecular basis of some naturally occurring and induced G. moniliformis mutants defective in fumonisin production. Here, we describe evidence for the molecular basis of one of these mutations at the genetically defined Fum3 locus. Deletion mutants of FUM9, a cluster gene predicted to encode a dioxygenase, produce only fumonisins B3 and B4, which lack a hydroxyl group at carbon 5. This is the same phenotype exhibited by strains with mutations in the Fum3 locus. We sequenced the region corresponding to FUM9 in a Fum3 mutant and identified a transition mutation that introduces a stop codon early in the FUM9 protein-coding region. Together the results indicate that the FUM9 gene is equivalent to the Fum3 locus. Currently, we are attempting to complement the Fum3 mutant by transformation with a wild-type FUM9 allele.