WEST LAFAYETTE, Ind. - Discovery that a specific gene is integral to both fungal invasion of corn and development of a potentially deadly toxin in the kernels may lead to ways to control the pathogen and the poison.
Purdue University researchers evaluated the fungal gene ZFR1 and found that it is vital to the process of the fungus growing on corn kernels. Production of the toxin decreased when the scientists disabled the gene.
At certain levels, the toxin can cause illness in humans and most domestic livestock. Horses and pigs are at particular risk and can develop fatal diseases by ingesting feed containing one of a group of toxins called fumonisins (few-mahn-ah-sins). About $40 million of the U.S. corn crop is lost annually due to presence of these toxins, according to experts.
"Our main research question has been what triggers toxin production when the fungus attacks the corn kernel; it appears that kernel starch plays an important role," said Charles Woloshuk, a Purdue plant pathologist. "When ZFR1 is deleted, the resulting mutant fungus has a problem transporting sugars that are produced from the degradation of kernel starch."
The resulting sugars must be transported to cells as fuel for other biochemical processes.
"The pathogen - the fungus Fusarium verticillioides - has a number of putative sugar transporter genes that are expressed during its growth on kernels and toxin production," Woloshuk said. "Disruption of ZFR1 also affects expression of the sugar transporter genes."
Woloshuk and his colleague, Bert Bluhm, now at the University of Arkansas, report in the current issue of Molecular Plant Pathology that when the gene ZFR1 is turned off, it reduces manifestation of genes involved in production of the most prevalent and dangerous fumonisin, FB1.
The researchers studied ZFR1 regulation of fungal growth and toxin production in the starch-rich areas of corn kernels and the conversion
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