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Lynda Ciuffetti
Professor and Department Chair, Botany and Plant Pathology
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RESEARCH:
A major goal of modern plant pathology is a molecular definition of factors that regulate fungal pathogenesis. We are investigating fungal pathogens which produce host-selective toxins (HST) because HSTs appear to be readily identifiable examples of fungal pathogenicity factors. HSTs, produced by at least 15 species of fungi, are unique metabolites believed to be involved in pathogenesis because they are toxic only to hosts susceptible to the fungus but not to resistant plants or nonhosts. Genetic analysis has established an absolute correlation between toxin production and pathogenicity (or high virulence) and lends additional support to the significance of HSTs in pathogenicity. Therefore, based on observations of the extreme specificity of these compounds and conventional genetic analyses of toxin production and pathogenicity, these toxins are believed to play a causal role in pathogenesis.
Pyrenophora tritici-repentis, causal agent of Tan Spot of Wheat, produces a host-specific toxin (Ptr toxin) which has been recently isolated and characterized as a protein. Because it is a protein, it is most likely the direct product of a single gene. The P. tritici-repentis-wheat system affords a unique situation for the isolation of a gene responsible for pathogenesis. Our efforts are directed toward the determination of the role of Ptr toxin in disease development. We are interested in cloning the gene for Ptr toxin production because we feel this is the most direct and conclusive approach. The fact that Ptr toxin is a protein and thus, the direct product of a gene, is very appealing because it greatly simplifies the cloning approach and subsequently, a direct molecular genetical analysis of the role of the HST in disease development. The cloned Ptr gene will be examined for its ability to confer the phenotype of toxin production and pathogenesis in nontoxin producing isolates of the fungus. Furthermore, cloning of the Ptr toxin gene would allow direct analysis at the nucleotide level of nonpathogenic isolates of P. tritici-repentis and related species to determine genetic dissimilarity. Hopefully, this would provide insights to the origin of Ptr toxin production and concurrently, pathogenicity.