Genetic 'Fix' For Problem In Some Sweet Corn Hybrids Developed

Several herbicides registered for use on sweet corn kill weeds but not the crop, thanks to protective enzymes in corn that rapidly degrade the chemicals. But some sweet corn hybrids aren't so lucky; they harbor a genetic defect that impedes the enzymes, causing herbicides to linger in the plants, which suffer stunted growth or other harm.

Now, with the defect known, plant breeders have begun using a technique called backcrossing to eliminate this herbicide-sensitivity from germplasm used to develop commercial hybrids. This should greatly reduce the risk of injury to sweet corn from registered herbicides, notes Marty Williams, an ecologist in the ARS Invasive Weed Management Research Unit in Urbana, Ill.

Together with UI colleague Jerald Pataky, Williams elaborates on the problem of herbicide sensitivity in sweet corn, and the benefits expected from discovering its genetic cause, in two articles in Weed Science. One article identifies the genetic cause of sensitivity to tembotrione, a new corn herbicide available this year. The other article—written with UI colleague Dean Riechers; Jon Nordby, formerly with UI; and General Mills' Joe Lutz—details the genetic basis of sensitivity to several existing herbicides.

The team found that a cytochrome P450 gene, which regulates metabolism of nicosulfuron and bentazon, is also responsible for protecting corn from other unrelated, P450-metabolized herbicides. By examining offspring plants derived from a cross between a herbicide-sensitive sweet corn inbred and a herbicide-tolerant inbred, they concluded that a defect in the P450-gene—or a very closely-linked P450 gene—results in damage to plants from five distinct herbicide classes.

The team's subsequent evaluations of 54 sweet corn hybrids and 40 inbred lines found the faulty P450 gene is widespread in both processing and fresh-market types of sweet corn grown throughout North America, but that it can eventually be eliminated with selective breeding.