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A discovery of a specific gene thatıs involved with both fungal invasionof corn and the development of a potentially deadly toxin in the kernels mayhelp researchers find a way to control them in the future.Purdue University researchers evaluated the fungal gene ZFR1 andobserved that toxin production decreased when they disabled the gene.At certain levels, the toxin can cause illness in humans and mostdomestic livestock. Horses and pigs are at particular risk and can developfatal diseases by ingesting feed containing one of a group of toxins calledfumonisins. Experts estimate the presence of these toxins cause a loss of$40 million to U.S. corn producers.Charles Woloshuk, a Purdue plant pathologist, as been looking into whattriggers toxin production when the fungus attacks the corn kernel.³It appears that kernel starch plays an important role," Woloshuk said."When ZFR1 is deleted, the resulting mutant fungus has a problemtransporting sugars, which are produced from starch degradation."These sugars must be transported to cells as fuel for other biochemicalprocesses."The pathogen - the fungus Fusarium verticillioides - has a number ofputative sugar transporter genes that are expressed during its growth onkernels and toxin production," Woloshuk said. "Disruption of ZFR1 alsoaffects expression of the sugar transporter genes."Woloshuk and his colleague Bert Bluhm, now at the University ofArkansas, report in the current issue of Molecular Plant Pathology that whenthe gene ZFR1 is turned off, it reduces manifestation of genes involved inproduction of the most prevalent and dangerous fumonisin, FB1.The researchers studied ZFR1 regulation of fungal growth and toxinproduction in the starch-rich areas of corn kernels and the conversion ofstarch to glucose, glucose recognition and the expression of sugartransporter genes. From this information, Woloshuk and his team identified aspecific sugar transporter, FST1 (fusarium sugar transporter1), that isnecessary for FB1 production.Although FST1 is required for FB1 production, it is not involved withthe fungus infecting corn kernels. This led the scientists to hypothesizethat FST1 acts as a molecular sensor necessary for toxin production.Kernels with lower starch content, most notably immature kernels, don'tsupport toxin production, Woloshuk said. This is evidence that the kernelmakeup dictates how this pathogen controls toxin production.Corn and fungal growth were unaffected when the sugar transporter genewas disrupted, but toxin production on the kernels was cut by about 82percent, 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 toxic cornbecause 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 soexpensive, however, that it usually isn't done unless the disease is highlyevident.Weather and insect damage impact development of a variety of fungi andtoxins and also influence the level of poisons that are present. Toxins aremore likely to develop in corn when hot, dry weather is followed by highlyhumid or wet weather.The group of toxins associated with varieties of fusarium species areknown as mycotoxins. Some clinical evidence links these toxins with certainhuman cancers. Grains grown for cereal and feeds are susceptible to one or more of thefusarium fungi species. Wheat and barley attacked by one of the speciesclosely related to Fusarium verticillioides can develop head blight andaccumulate mycotoxins, causing billions of dollars in crop losses worldwide.Further study is needed because the researchers still don't know whattriggers the biochemical process that regulates ZFR1 and consequently leadsto toxin production, Woloshuk said. The scientists also are investigatingthe sugar transporter genes to discover if they have other roles in thefungus and what molecular interactions between the fungus and the plantallow infection and toxin production."We're closer to finding some of the triggers in corn that assist thefungus in toxin production," Woloshuk said.The other researchers involved in this study were Department of Botanyand Plant Pathology doctoral student Hun Kim and Robert Butchko of the USDANational Center for Agricultural Utilization Research Service in Peoria,Ill. Bluhm is a former graduate student in Woloshuk's laboratory whorecently joined the University of Arkansas faculty as an assistantprofessor.A USDA-National Research Initiative grant provided support for thiswork.

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