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Defining gene's role may lead to prevention of dangerous corn toxin

of starch to glucose, glucose recognition and the expression of sugar transporter genes. From this information, Woloshuk and his team identified a specific sugar transporter, FST1 (fusarium sugar transporter1), that is necessary for FB1 production.

Although FST1 is required for FB1 production, it is not involved with the fungus infecting corn kernels. This led the scientists to hypothesize that FST1 acts as a molecular sensor necessary for toxin production.

Kernels with lower starch content, most notably immature kernels, don't support toxin production, Woloshuk said. This is evidence that the kernel makeup dictates how this pathogen controls toxin production.

Corn and fungal growth were unaffected when the sugar transporter gene was disrupted, but toxin production on the kernels was cut by about 82 percent, Woloshuk said.

When fusarium invades corn in the field, it causes an ear rot disease. Even knowing that ear rot is present doesn't help identify corn containing toxin because obvious signs of the fungus don't correlate with presence of toxins. The only way to confirm toxin is present is to test for it. Testing is so expensive, however, that it usually isn't done unless the disease is highly evident.

Weather and insect damage impact development of a variety of fungi and toxins and also influence the level of poisons that are present. Toxins are more likely to develop in corn when hot, dry weather is followed by highly humid or wet weather.

The group of toxins associated with varieties of fusarium species are known as mycotoxins. Some clinical evidence links these toxins with certain human cancers.

Grains grown for cereal and feeds are susceptible to one or more of the fusarium fungi species. Wheat and barley attacked by one of the species closely related to Fusarium verticillioides can develop head blight and accumulate mycotoxins, causing billions of dollars in crop losses worldwide.


Contact: Susan A. Steeves
Purdue University

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