Submitted to: National Cotton Council Beltwide Cotton Conference
Publication Type: Abstract Only
Publication Acceptance Date: November 3, 2011
Publication Date: N/A
Technical Abstract: A genetically unique strain of the Fusarium wilt pathogen was first recognized in wilted and dead Upland cotton seedlings in Australia in 1993. Since that time the disease spread rapidly despite stringent containment practices. The Australian biotype isolates of Fusarium oxysporum f. sp. vasinfectum (Fov) produce copious amount of fusaric acid in potato dextrose cultures and their virulence was directly correlated to amounts of fusaric acid produced. Though fusaric acid has long been implicated in the pathogenesis of Fusarium wilt for a number of other plant species including tomato, watermelon, and flax, direct evidence for the role of fusaric acid in the virulence is still lacking as the biosynthetic enzymes and genes for fusaric acid have not been identified and cloned. We set out to identify and clone the polyketide synthase (PKS) gene involved in the fusaric acid biosynthesis through differential display. We identified a partial clone whose expression matched the expected profile of the fusaric acid production in the fungus. Using homology based strategy, we cloned a gene cluster containing the PKS gene as well as an amino acid kinase gene and the corresponding cDNAs. Targeted gene disruption of either of these genes in the Australian biotype Fov isolate resulted in complete blockage of fusaric acid production. These fusaric acid knockout mutants showed much weaker pathogenicity than their wild type progenitor toward tomato seedlings in a seedling germination bioassay on agar plates. These results indicate that fusaric acid plays an important role in the pathogenicity of the Australian biotype isolates.