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ARS Home » Midwest Area » Urbana, Illinois » Global Change and Photosynthesis Research » Research » Publications at this Location » Publication #215995
Title: Genetic Basis of Sensitivity in Sweet Corn to Tembotrione

Author
item Williams, Martin
item PATAKY, JERALD - UNIV OF ILLINOIS

Submitted to: Weed Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/10/2008
Publication Date: 5/16/2008
Citation: Williams, M., Pataky, J.K. 2008. Genetic Basis of Sensitivity in Sweet Corn to Tembotrione. Weed Science. 56:364-370.

Interpretive Summary: Herbicides are one tool to manage weeds in sweet corn; however, crop injury from herbicide use is an ongoing problem in sweet corn production. A wide range of responses to many postemergence herbicides occurs among more than 600 commercially-available sweet corn hybrids, and because of this variation, the replacement of antiquated herbicide chemistry with new postemergence herbicides in sweet corn is limited. A newly emerging herbicide not presently registered for use in sweet corn (AE 0172747) appears safe on many but not all hybrids. This research explored the genetic basis for sensitivity of sweet corn to AE 0172747. A single recessive gene appears to condition sensitivity to AE 0172747, and it is the same gene or a closely linked gene that also confers sensitivity to several other postemergence herbicides. This work provides an understanding of the genetics of sweet corn sensitivity to AE 0172747 and shows how that sensitivity relates to knowledge of other herbicides. The impact is that this knowledge can be used to reduce risk of herbicide use in sweet corn, by helping plant breeders identify and eliminate sensitive germplasm, and by helping herbicide manufacturers construct pesticide labels that address the risk of herbicide use. The growers will benefit because of improved crop and weed management.

Technical Abstract: Field studies were used to 1) test the hypothesis that the genetic basis of sweet corn sensitivity to AE 0172747 is the same recessive gene that conditions sensitivity to mesotrione, and 2) compare the extent of early-season herbicide injury from AE 0172747 and mesotrione on sweet corn hybrids and inbreds. The first objective was tested using a total of 136 S2 families (>6,000 S4 plants total) derived from a cross of a mesotrione-sensitive inbred and a mesotrione-tolerant inbred. The number of S4 plants with (>50% leaf area chlorotic or bleached) and without injury symptoms in each family were used to classify plants as sensitive, segregating, and tolerant seven days after application of 184 g AE 0172747 per hectare at the four- to five-leaf stage. Based on Chi-square goodness of fit tests, responses of families both years fit a 3 sensitive : 2 segregating : 3 tolerant ratio (p = 0.36), which would be the expected segregation pattern if sensitivity to AE 0172747 was conditioned by a single recessive gene. When family responses were compared to previous research on sensitivity to mesotrione, an association was evident among S2 families responses, as evidenced by 88% of families having same responses to both herbicides and correlation (0.924) between percent of plants in families sensitive to AE 0172747 and mesotrione. The second objective was tested in six field experiments by quantifying the extent of early-season injury to 249 sweet corn hybrids and 58 sweet corn inbreds from application of AE 0172747 (184 g ai per hectare) or mesotrione (210 g ai per hectare). An association between sensitivity to AE 0172747 and mesotrione was also evident among sweet corn hybrids and inbreds; most germplasm had minimal (<10%) injury from both herbicides, while seven hybrids were severely (>50%) injured or killed by both herbicides. Responses of hybrids to AE 0172747 and mesotrione followed a distinct pattern for hybrids that previously were identified as being homozygous for alleles at a locus on chromosome 5S conditioning sensitivity to nicosulfuron and mesotrione, homozygous for alleles conditioning tolerance to these two herbicides or heterozygous. For instance, under no circumstances did homozygous recessive germplasm avoid severe injury, while injury to homozygous dominant germplasm was always <5%. Based on segregation of responses of S2 families, correlation among family responses to AE 0172747 and mesotrione, and association between responses of hybrids and inbreds to both herbicides, we conclude that the single recessive gene that conditions sensitivity to AE 0172747 is the same gene or a closely linked gene that conditions sensitivity to mesotrione and several other postemergence herbicides.