Factors Affecting Differential Sensitivity of Sweet Corn to HPPD-Inhibiting Herbicides Martin M

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Factors Affecting Differential Sensitivity of Sweet Corn to HPPD-Inhibiting Herbicides Martin M Weed Science 2010 58:289–294 Factors Affecting Differential Sensitivity of Sweet Corn to HPPD-Inhibiting Herbicides Martin M. Williams II and Jerald K. Pataky* Mutation of a cytochrome P450 (CYP) allele on the short arm of chromosome 5 affects sensitivity in sweet corn to mesotrione and to tembotrione plus isoxadifen applied POST. Hybrids that are homozygous for the functional allele (i.e., CYPCYP) are rarely injured at registered use rates, hybrids that are homozygous for mutant alleles (i.e., cypcyp) are frequently injured, and hybrids that are heterozygous for a functional and mutant allele (i.e., CYPcyp) have more variable responses over trials. The objectives of this work were (1) to conduct side-by-side comparisons of sweet corn hybrid responses to mesotrione, tembotrione plus isoxadifen, and topramezone under field conditions; and (2) to compare dose– response relationships among CYPCYP, CYPcyp, and cypcyp hybrids. Among 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitors used POST in sweet corn, topramezone was safe on the 746 hybrids tested. When environmental conditions favored crop growth, mesotrione injured the largest number of hybrids, and these hybrids were almost exclusively cypcyp or CYPcyp. The safener isoxadifen added to the tembotrione product greatly reduced occurrence of injury to the CYPcyp genotypic class but not to the cypcyp hybrids. Despite a common genetic basis for herbicide metabolism, genotypic classes of sweet corn hybrids did not have identical field responses to mesotrione, tembotrione plus isoxadifen, and topramezone. Nomenclature: Isoxadifen, ethyl-5, 5-diphenyl-2-isoxazoline-3-3-carboxylate; mesotrione; tembotrione; topramezone; sweet corn, Zea mays L. Key words: Cross-sensitivity, cytochrome P450, dose–response, herbicide tolerance, nsf1 gene. In recent years, several new herbicides that inhibit 4- trials, a more complete assessment of the crop injury risks hydroxyphenylpyruvate dioxygenase (HPPD) have become associated with use of these herbicides is warranted. available for POST broadleaf and grass weed control in sweet Cytochrome P450 (CYP) enzymes are a major family of corn. Competitive inhibition of the HPPD enzyme, involved monooxygenase enzymes responsible for metabolism of many in carotenoid biosynthesis, ultimately leads to oxidative herbicides, thus conferring selectivity in crops (Barrett 2000). degradation of chlorophyll and photosynthetic membranes Mutation of a CYP gene on the short arm of chromosome 5, in growing shoot tissues. Chloroplast synthesis and function referred to as the nsf1 or ben1 gene in previous research, are compromised, and susceptible plants often have bleached conditions sensitivity to multiple P450-metabolized herbi- leaves 1 wk after POST application. As of 2009, there were no cides, including nicosulfuron (Williams et al. 2006), reported biotypes of weed species resistant to HPPD- mesotrione (Nordby et al. 2008), and tembotrione plus inhibiting herbicides (Heap 2009). In addition to contribut- isoxadifen (Williams and Pataky 2008). The functional allele ing to the management of herbicide-resistant weed popula- at this CYP locus conditions responses to several other P450- tions, the HPPD-inhibiting herbicides provide options for metabolized herbicides with various modes of action (Nordby POST control of some grasses in sweet corn. et al. 2008) and appears to be the ‘‘super P450’’ proposed by Three HPPD-inhibiting herbicides are currently registered Barrett (Barrett et al. 1994). The mutant allele of this CYP for use in the United States for sweet corn production. gene (or closely linked CYP genes) was found in hybrids and Mesotrione, labeled in 2005, is a member of the benzoylcy- inbreds from every major food processor and seed company in clohexane-1,3-dione family of herbicides (Mitchell et al. the sweet corn industry (Pataky et al. 2009), revealing an 2001). Topramezone, labeled in 2006, is a member of the industry-wide occurrence of herbicide sensitivity in sweet benzoyl pyrazole herbicide family (Grossman and Ehrhardt corn. 2007). Tembotrione, labeled in 2008, is a member of the Despite a common genetic basis of sensitivity to mesotrione triketone herbicide family (USEPA 2007). The commercial and tembotrione plus isoxadifen, response to these two formulation of tembotrione includes a safener, isoxadifen herbicides was not identical within genotypic classes of the (ethyl-5, 5-diphenyl-2-isoxazoline-3-3-carboxylate), in a 2 : 1 CYP gene (Williams and Pataky 2008). Hybrids homozygous ratio by weight. Differential tolerance among hybrids has been for functional alleles (i.e., CYPCYP) were uninjured or evaluated for HPPD-inhibiting herbicides individually sustained minor injury from either herbicide. Hybrids (O’Sullivan et al. 2002; Soltani et al. 2007). Sweet corn homozygous for mutant alleles (i.e., cypcyp) were severely . hybrids have been tested for response to all three herbicides injured ( 50%) by both herbicides. Most hybrids heterozy- gous for a functional and a mutant allele (i.e., CYPcyp) were under common field conditions in only a single study moderately (. 10 to 50%) injured by mesotrione but showed (Bollman et al. 2008). Because only six to nine of the no injury from tembotrione plus isoxadifen. In other research, approximately 600 commercial sweet corn hybrids grown no hybrids were injured by topramezone, including cypcyp throughout North America were evaluated in any of those hybrids (i.e., ‘DelMonte 20–38’, ‘Merit’; Bollman et al. 2008; Soltani et al. 2007). An understanding of the variable DOI: 10.1614/WS-D-09-00058.1 responses of hybrids with mutant CYP alleles to the HPPD- * U.S. Department of Agriculture–Agricultural Research Service, Global inhibiting herbicides and the effects of isoxadifen in relation Change and Photosynthesis Research, University of Illinois, 1102 S. Goodwin Avenue, Urbana, IL 61801; and Department of Crop Sciences, University of to the genotypic class remain unresolved. Illinois, 1102 S. Goodwin Avenue, Urbana, IL 61801. Corresponding author’s Advances in the knowledge of sweet corn sensitivity to E-mail: [email protected] herbicides have enabled sweet corn breeders to begin Williams and Pataky: HPPD inhibitors on sweet corn N 289 eliminating mutant CYP alleles from inbreds to avoid with 202 kg N ha21 at 2 to 3 wk before planting. Preplant sensitivity among future hybrids; however, elimination of tillage included two passes each of a field cultivator and these alleles in commercial germplasm will require several spring-tine harrow. Early season weeds were controlled with a generations of testing and selection. In the meantime, weeds PRE application of atrazine at 2.2 kg ai ha21 plus S- remain a serious problem, and POST herbicides are used metolachlor at 1.8 kg ai ha21. Seeds were planted on May 29 widely. Mesotrione, tembotrione plus isoxadifen, and topra- during both years. Each herbicide was applied at 23 mezone are among the newest weed control tools available to registered use rates using a tractor-mounted, compressed-air sweet corn growers. Although weed control efficacy of these sprayer equipped with nozzles delivering 187 L ha21 of water herbicides has received considerable attention, herbicide at 276 kPa when sweet corn had four to five visible leaf collars. manufacturers, seed companies, extension personnel, and Rates of the commercial formulation of herbicides were growers have little information upon which to base mesotrione2 at 210 g ai ha21, tembotrione3 at 184 g ai ha21 2 2 recommendations for hybrid tolerance to the above three (with 96 g isoxadifen ha 1), and topramezone4 at 36 g ai ha 1. herbicides. Adjuvants included 1% (v/v) crop oil concentrate (COC) in Our goal was to use knowledge of the recently discovered 2008 and 1% (v/v) COC plus 2% (v/v) urea ammonium genetic basis of sweet corn cross-sensitivity (Nordby et al. nitrate (UAN, with 28% nitrogen) in 2009. Plants were 2008; Pataky et al. 2008, 2009; Williams and Pataky 2008; evaluated visually 1 and 3 wk after treatment (WAT) for Williams et al. 2008), in combination with a more percentage of leaf bleaching. Mean responses of all hybrids to comprehensive examination of sweet corn germplasm, to mesotrione, tembotrione plus isoxadifen, and topramezone provide a greater understanding of the risks associated with were summarized, including comparisons of the hybrids with using HPPD-inhibiting herbicides POST in sweet corn their genotype characterized at the CYP locus. Because not all production. We wanted to test the hypothesis that differences hybrids were available both years, data are presented separately in CYP genotypes is a factor in the degree of injury (i.e., leaf by year. bleaching) to sweet corn hybrids treated with HPPD- inhibiting herbicides. Therefore, our objectives were (1) to Dose–Response. Responses of each genotypic class (i.e., conduct a side-by-side comparison of sweet corn hybrid CYPCYP, CYPcyp, and cypcyp) were evaluated in dose– response to mesotrione, tembotrione plus isoxadifen, and response studies in the greenhouse using near-isogenic topramezone under field conditions; and (2) to quantify dose– hybrids. Near-isogenic hybrids were made from two pairs of response relationships among CYPCYP, CYPcyp, and cypcyp inbred lines selected in the S6 generation for functional (CYP) hybrids. or mutant (cyp) alleles. In addition to mesotrione, tembo- trione plus isoxadifen, and topramezone, a formulation of tembotrione without the safener was included. Each herbicide Materials and Methods was a separate trial, and
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