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Some sweet corn (Zea mays L.) hybrids and inbreds can be severely injured or killed after postemergence applications of certain P450-metabolized herbicides. Consequently, existing hybrids are regularly evaluated for tolerance to new herbicides, and new hybrids are evaluated for tolerance to existing herbicides. In 2005 and 2006, the University of Wisconsin Cooperative Extension Service coordinated 12 trials in six states in which a total of 149 sweet corn hybrids were evaluated for tolerance to three cytochrome P450-metabolized herbicides: nicosulfuron, foramsulfuron, and mesotrione. Hybrid responses differed substantially within and among locations. The objective of this study was to determine if alleles affecting herbicide sensitivity (e.g., cytochrome P450 alleles) were associated with differences in levels of injury to sweet corn hybrids in these trials. Based on responses of F₂ progeny to nicosulfuron, foramsulfuron, and mesotrione, 95 hybrids were classified as homozygous for alleles conditioning herbicide tolerance; 47 hybrids were classified as heterozygous with one allele each conditioning tolerance and sensitivity; and two hybrids were classified as homozygous for alleles conditioning sensitivity. When trial mean levels of injury after applications of mesotrione, nicosulfuron, and foramsulfuron in the herbicide trials were above 1%, 4%, and 5%, respectively, the response of the three genotypic classes of hybrids followed a consistent pattern. Homozygous-sensitive hybrids were injured most severely and often were killed by the two acetolactate synththase-inhibiting herbicides, nicosulfuron and foramsulfuron. Heterozygous hybrids had an intermediate response to all three herbicides that was more similar to homozygous-tolerant hybrids than homozygous-sensitive hybrids; however, injury to heterozygous hybrids was 1.5 to 2.3 times greater and significantly (P < 0.05) different from homozygous-tolerant hybrids based on t tests of group means and comparisons of predicted values from regressions of genotypic means on trial means. Based on responses of the 149 hybrids in this trial, the potential for and level of crop injury from use of nicosulfuron, mesotrione, and foramsulfuron on any specific sweet corn hybrid is conditioned largely by alleles at a single locus.

Recently, claims have been made that the use of glyphosate and transgenic crop traits increases plant susceptibility to pathogens. Transgenic traits used widely for years in dent corn are now available in commercial sweet corn cultivars, specifically, the combination of glyphosate resistance (GR) and Lepidoptera control (Bt). The objective was to assess the interactions of the GR+Bt trait, glyphosate, and Goss’s wilt on sweet corn. Nine treatments were tested under weed-free conditions at two sites in 2013 and 2014. Treatments included two isogenic cultivars differing only in the presence or absence of GR+Bt, with and without postemergence application of glyphosate, and inoculation with the causal agent of Goss’s wilt (Clavibacter michiganensis ssp. nebraskensis) before glyphosate application, after glyphosate application, or no inoculation. Results failed to show glyphosate or the GR+Bt trait influenced sweet corn susceptibility to Goss’s wilt. The only factor affecting Goss’s wilt incidence was whether plants were inoculated with C. michiganensis ssp. nebraskensis. In the absence of glyphosate application, yet under weed-free conditions, several yield traits were higher in sweet corn with the GR+Bt trait. Results showed that the GR transgene confers the same level of tolerance to glyphosate in sweet corn as observed previously in dent corn. If true, recent claims about glyphosate and transgenic traits increasing plant disease would be of major concern in sweet corn; however, no relationships were found between the GR+Bt trait and/or glyphosate to Goss’s wilt incidence in sweet corn.

Some sweet corn (Zea mays L.) hybrids and inbreds can be severely injured by applications of postemergence herbicides. An association was observed between the responses of sweet corn hybrids and inbreds to nicosulfuron and mesotrione, and F₂ families derived from a cross of a sensitive (Cr1) and a tolerant (Cr2) sweet corn inbred segregated for response to these two herbicides. These observations prompted us to examine the inheritance of sensitivity in sweet corn to multiple postemergence herbicide treatments with different modes of action and to determine if there was a common genetic basis for cross-sensitivity to these herbicides. The sensitive and tolerant inbreds, progeny in the F₁, F₂, BC₁, and BC₂ generations, and BC₁S₁, BC₂S₁, F_2:3 (S_1:2) and F_3:4 (S_2:3) families were screened for responses to eight herbicide treatments. Based on segregation of tolerant and sensitive progeny and segregation of family responses, our data indicate that a single recessive gene in Cr1 conditioned sensitivity to four acetolactate synthase (ALS)-inhibiting herbicides (foramsulfuron, nicosulfuron, primisulfuron, and rimsulfuron), a 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicide (mesotrione), a growth regulator herbicide combination (dicamba + diflufenzopyr), and a protoporphyrinogen oxidase (PPO)-inhibiting herbicide (carfentrazone). Based on highly significant positive correlations of phenotypic responses among BC₁S₁, BC₂S₁, F_2:3, and F_3:4 families, the same gene (or closely linked genes) appeared to condition responses to each of these herbicide treatments. The dominant allele also conditions tolerance to bentazon [a photosystem II (PSII)-inhibiting herbicide] although another gene(s) also appeared to affect bentazon tolerance.

Mutation of a cytochrome P450 (CYP) gene on the short arm of chromosome five, referred to as nsf1 or ben1, conditions sensitivity to certain P450-metabolized herbicides in corn (Zea mays L.). Previous research has shown that the sweet corn inbred Cr1 is sensitive to nicosulfuron, mesotrione, and at least seven other P450-metabolized herbicides with five different modes of action. Although the nsf1/ben1 CYP gene has not been sequenced from Cr1, a QTL that conditions cross-sensitivity to P450-metabolized herbicides was detected in a segregating population of Cr1 × Cr2 (herbicide tolerant) on the short arm chromosome five in tight linkage disequilibrium with the nsf1/ben1 CYP locus. Sweet corn hybrid cultivars and inbreds that had been identified in previous research as being susceptible to injury from P450-metabolized herbicides were tested in this study to determine if they were allelic with Cr1 for cross-sensitivity to nicosulfuron and mesotrione. These cultivars and inbreds were developed by 12 independent commercial breeding programs. These cultivars include sugary, sugary enhancer, and shrunken-2 endosperm types that are grown for processing and fresh consumption in markets throughout North America and in other temperate climates throughout the world. Each hybrid cultivar, their F₂ progeny, and progeny from testcrosses of cultivars with Cr1 and Cr2 were evaluated for responses to mesotrione and nicosulfuron. Each inbred line, progeny from crosses of inbreds with Cr1 and Cr2, and F₂ progeny from crosses of inbreds with Cr1 were also tested. Based on segregation of progeny from testcrosses with Cr1 and Cr2 and the F₂ generation, 45 sweet corn hybrid cultivars and 29 sweet corn inbreds, including lines from each of the 12 breeding programs, appeared to be sensitive to nicosulfuron and mesotrione as the result of a gene that is the same as or very closely linked to the gene in Cr1. None of the cultivars or inbreds appeared to be sensitive to these herbicides as a result of other independent genes; however, additional genes that modify responses to these herbicides may be present in a few cases. The presence of a gene conditioning sensitivity to nicosulfuron and mesotrione, and probably to several other P450-metablolized herbicides, provides an explanation for varied levels of injury and inconsistent responses of sweet corn hybrid cultivars under differing environmental conditions. This information provides a basis from which an industry-wide concern with herbicide sensitivity in sweet corn can be addressed by various methods, including the elimination of an allele rendering germplasm sensitive.

Nicosulfuron and mesotrione are herbicides from different chemical families with different modes of action. An association between the sensitivity of sweet corn (Zea mays L.) to nicosulfuron and mesotrione was observed when hybrids, inbreds, and S₁ families (S₂ plants) were evaluated for herbicide sensitivity in field trials. In 2003 and 2004, 50% and 53% of mesotrione-sensitive hybrids were sensitive to nicosulfuron compared with only 6% and 1% of mesotrione-tolerant hybrids that were sensitive to nicosulfuron. In trials with inbreds in 2003 and 2004, 88% and 78% of nicosulfuron-sensitive inbreds had some injury from mesotrione but 0% and 5% of nicosulfuron-tolerant inbreds were injured by mesotrione. Among S₁ families, 77% of the mesotrione-sensitive families were nicosulfuron-sensitive but only 5% of the mesotrione-tolerant families were sensitive to nicosulfuron. Segregation of S₁ families for response to mesotrione was not significantly different from a 1:2:1 pattern of sensitive: segregating: tolerant families (chi square value = 2.25, P = 0.324) which would be expected if sensitivity was conditioned by a single recessive gene. Segregation of S₁ families for response to nicosulfuron was 15:23:26 (sensitive: segregating: tolerant) which was slightly different from an expected 1:2:1 ratio (chi square value = 8.84, P = 0.012). Segregation of S₁ families probably was affected by the relatively small number of S₂ plants sampled from each family. Similar responses of the S₁ families to nicosulfuron and mesotrione lead us to hypothesize that the same recessive gene is conditioning sensitivity to both herbicides. Possibly, this gene is common in the inbreds and hybrids that were sensitive in these trials. These hypotheses will be tested by examining segregation in S₂ families and other segregating generations and by conducting tests of allelism among sensitive inbreds and inbred parents of sensitive hybrids. Chemical names: 2-(4-mesyl-2-nitrobenzoyl)-3-hydroxycyclohex-2-enone, (mesotrione); 2-[[[[(4,6-dimethoxy-2-pyrimidinyl)amino]carbonyl]amino]sulfonyl]-N,N-dimethyl-3-pyridinecarboxamide, (nicosulfuron).