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ARS Home » Research » Publications at this Location » Publication #77904


item Proctor, Robert
item Hohn, Thomas
item McCormick, Susan

Submitted to: Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/9/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary: The objective of this study was to determine whether the ability of the fungus Gibberella zeae to produce trichothecene toxins contributes to its ability to cause disease on wheat. Previously, we demonstrated that mutants of the fungus that were unable to produce the toxins caused less disease. Here, we demonstrated, via two genetic techniques, that when mutants regained toxin production they also regained the ability to cause high levels of disease on wheat seedlings. These results indicate that trichothecene toxin production by G. zeae enhances the ability of the fungus to cause disease and suggest that disease control might be obtained by developing wheat with high resistance to the toxins.

Technical Abstract: Gibberella zeae is a pathogen of small grains and produces trichothecene mycotoxins in infected host tissue. The role of trichothecenes in the virulence of G. zeae was previously investigated using trichothecene-deficient mutants generated via transformation-mediated disruption of a gene (Tri5) encoding the first enzyme in trichothecene biosynthesis. The mutants were less virulent on wheat (cv. Wheaton) than the wild-type strain from which they were derived. Here, we used two approaches to determine whether the reduced virulence of mutants was due specifically to Tri5 disruption or to nontarget effects caused by the transformation process. First, we generated a revertant from a Tri5 disruption mutant by allowing the mutant to pass through its sexual phase. Second, we complemented the Tri5 mutation in a disruption mutant by transforming the mutant with a plasmid carrying a functional copy of Tri5. In all transformants examined, the ability to produce trichothecenes was restored. The restoration of trichothecene production in the revertant progeny and the complemented mutant was accompanied by restoration of wild-type or near wild-type levels of virulence on wheat seedlings. The results indicate that the reduced virulence of the mutants was caused by disruption of Tri5 rather than nontarget effects resulting from transformation. The results also provide further evidence that trichothecenes contribute to the virulence of plant pathogenic fungi.