| Don White
Department of Crop Sciences
(217) 333-1093; email@example.com
Department of Crop Sciences
(217) 333-3098; firstname.lastname@example.org
Fusarium ear rot of corn has become an important disease of dent corn in the midwestern United States even though the disease damages a very low percentage of kernels. However, the fungi that cause the disease produce fumonisin mycotoxins that have been linked to serious animal and human health disorders, including human esophageal cancer and neural tube birth defects (Figure 1). Fumonisin can be common in corn grain in which there are few or no symptoms of Fusarium kernel rot.
Figure 1. Symptoms of Fusarium kernel rot and fumonisin-induced neural tube birth defects of mice.
On November 9, 2001, the United States Food and Drug Administration issued a “Guidance for Industry” for fumonisin levels of 2 to 4µg/g in human food and animal feeds. Importers of U.S. corn grain also are considering regulation of fumonisin. Whether “Guidance for Industry” will remain in effect or change to “Advisory” or “Action” levels is unknown. Concerns of drastic effects on corn markets and the possibility of undue public concern over consumption of food-based corn has slowed action by the FDA. Concentrations of fumonisin typically detected in corn grain could disrupt corn markets in Illinois one out of three years if “Action” levels as high as 5µg/g (the level safe for horses) are adopted.
Numerous studies have suggested that fumonisin is most likely to occur at levels of concern as a result of hot, dry environments at or before flowering. In 2001, we detected 14µg/g fumonisin in grain of a food-grade hybrid grown in the Illinois Commercial Trials near Dwight. Grain of many other commercial food-grade hybrids in that trial had fumonisin levels greater than 4µg/g. A food processor in Texas reported fumonisin concentrations greater than 5µg/g in corn grain produced in central Illinois in 2001.
In an effort to respond to this potentially serious threat to corn markets for Illinois farmers, we have used funding from Illinois C-FAR and USDA/CSREES-NRI-Food Safety to accomplish three objectives. First, we developed an inoculation technique that allows evaluation of a large number of different genotypes in central Illinois each summer. Second, we evaluated a set of food-grade corn hybrids and a select group of sweet corn hybrids and identified those most likely to have high levels of fumonisin. Third, we evaluated 1,589 inbreds crossed with FR1064 (a widely used commercial inbred) following inoculation at Urbana, Illinois and natural infection at two locations in North Carolina (Ponzer and Winterville). Fumonisin concentrations in corn grain ranged from 2 to 180µg/g (mean 23µg/g), 2 to 63µg/g (mean 15µg/g), and 1 to 237µg/g (mean 13µg/g) in Urbana, Ponzer, and Winterville respectively. We selected 11 inbreds with high levels of resistance, but they were not immune. For example, in inoculated experiments in 2001, one inbred source of resistance had 1.8µg/g fumonisin in grain from three replicates in two locations (Urbana and southern Indiana) compared to 99.3µg/g for FR1064 and 3µg/g for the source of resistance x FR1064.
It seems highly likely that we have identified sources of resistance to Fusarium ear rot and fumonisin production that will lead to control of fumonisin in corn grain in Illinois in most years.
Our next objectives are to determine inheritance of resistance and to identify molecular markers associated with resistance to facilitate incorporation of resistance into commercially used inbreds and hybrids. Successful completion of these objectives will depend on continued funding from sources such as Illinois C-FAR, which has been drastically reduced.
College of Agriculture, Consumer and Environmental Sciences
University of Illinois Extension
© 2002 University of Illinois
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