|Glenn, Anthony - Tony|
Submitted to: Multicrop Aflatoxin and Fumonisin Elimination and Fungal Genomics Workshop-The Peanut Foundation
Publication Type: Proceedings
Publication Acceptance Date: 10/24/2007
Publication Date: 10/24/2007
Citation: Glenn, A.E., Zitomer, N.C., Riley, R.T., Proctor, R. 2007. Characterization and complementation of an apparent FUM gene cluster deletion in Fusarium verticillioides. In: Proceedings of the Aflatoxin/Fumonisin Elimination and Fungal Genomics Workshop-The Peanut Foundation. October 22 - 24, 2007. Atlanta, GA. p. 40
Interpretive Summary: Abstract - no interpretive summary required.
Technical Abstract: The filamentous ascomycete Fusarium verticillioides is a worldwide pathogen of maize and produces the fumonisin mycotoxins. Contamination of maize kernels with fumonisin B1 (FB1) is of significant concern because of its causal role in equine leukoencephalomalacia, porcine pulmonary edema, liver and renal carcinogenicity in laboratory rodents, and possible human carcinogenicity and neural tube birth defects. Fumonisins B2, B3, and B4 (FB2, FB3, and FB4) also occur in maize but usually at concentrations lower than FB1. Most maize isolates of F. verticillioides produce the full complement of fumonisins. However a distinct population of F. verticillioides is pathogenic on banana and does not produce fumonisins. Fumonisin-producing strains from maize cause leaf lesions, developmental abnormalities, stunting, and sometimes death of maize seedlings (e.g., ‘Silver Queen’ hybrid), whereas fumonisin-nonproducing banana strains do not. Seedlings of Silver Queen inoculated with banana strains of F. verticillioides generally appear equivalent to uninoculated control seedlings. Production of fumonisins by F. verticillioides is dependent on a biosynthetic gene (FUM) cluster of 16 contiguous and co-expressed genes encompassing ~45.7 kb on chromosome 1. A Southern analysis of banana strains did not detect genes in the FUM cluster but did detect genes flanking the cluster. Nucleotide sequence analysis of the genomic region carrying the flanking genes revealed that the FUM cluster was absent in banana strains except for portions of FUM21 and FUM19, which are the terminal genes at each end of the cluster. The remnants of these two genes were contiguous, suggesting that 43.9 kb of the FUM cluster was presumably deleted. PCR analysis of the FUM21-FUM19 junction confirmed absence of the cluster in all banana strains examined. Cotransformation of banana strain NRRL 25059 with two overlapping cosmids (Cos6B and Cos4-5), which together contain the entire FUM cluster, yielded fumonisin-producing transformants that were pathogenic on maize seedlings. Conversely, maize strains that possess the FUM cluster but do not produce fumonisins because of mutations in FUM1, a polyketide synthase gene, were not pathogenic on maize seedlings. Together, the data indicate that fumonisin production may have been lost by deletion of the FUM cluster in the banana population of F. verticillioides but that fumonisin production could be restored by molecular genetic complementation. The results also indicate that fumonisin production by F. verticillioides is required for development of foliar disease symptoms on maize seedlings. However, the overall incidence and severity of seedling disease development are likely dependent on both the maize genotype and the amount of fumonisin produced by F. verticillioides strains.