The southern corn leaf blight epidemic of 1970 caused estimated losses of about 16% for the U.S. corn crop, equivalent to about $8 billion in current terms. The epidemic was caused by the prevalence of Texas male sterile cytoplasm (cms-T), used to produce most of the hybrid corn seed planted that year, combined with the emergence of a novel race of the fungus Cochliobolus heterostrophus that was exquisitely virulent on cms-T corn. Remarkably, the epidemic lasted just a single year. This episode has often been portrayed in the literature and textbooks over the last 50 years as a catastrophic mistake perpetrated by corn breeders and seed companies of the time who did not understand or account for the dangers of crop genetic uniformity. In this perspective article, we aim to present an alternative interpretation of these events. First, we contend that, rather than being caused by a grievous error on the part of the corn breeding and seed industry, this epidemic was a particularly unfortunate, unusual, and unlucky consequence of a technological advancement intended to improve the efficiency of corn seed production for America's farmers. Second, we tell the story of the resolution of the epidemic as an example of timely, meticulously applied research in the public sector for the public good.

Pantoea stewartii subsp. stewartii (syn. Erwinia stewartii) is the causal agent of Stewart's wilt or Stewart's disease of maize, which is endemic to the mid-Atlantic and Ohio River Valley regions of the United States. Seed transmission is rare. P. stewartii subsp. stewartii is a nonmotile, gram-negative, rod-shaped bacterium that enters leaves through feeding wounds made by Chaetocnema pulicaria, the primary insect vector and overwintering host for the pathogen. Disease symptoms, management methods, and a protocol for pathogen detection are included in this chapter.

Postemergence (POST) application of 4-hydroxyphenyl pyruvate dioxygenase (HPPD) inhibitors in combination with a photosystem II (PSII) inhibitor, such as atrazine [6-chloro-N-ethyl-N9-(1-methylethyl)-1,3,5-triazine-2,4-diamine], is common practice in sweet corn (Zea mays L.) production. Given the sensitivity of sweet corn to HPPD-inhibiting herbicides, the objective of this work was to determine the extent to which cytochrome P450 (CYP) genotype and PSII-inhibitors affect crop sensitivity to HPPD-inhibiting herbicides. Greenhouse experiments were used to identify PSII-inhibitors that were least injurious when combined with the HPPD-inhibitors, mesotrione [2-(4-mesyl-2-nitrobenzoyl)-3-hydroxycylohex-2-enone], tembotrione {2-[2-chloro-4-(methylsulfonyl)-3-[(2,2,2-trifluoroethoxy) methyl] benzoyl]-1,3-cyclohexanedione}, and topramezone {[3-(4,5-dihydro-3-isoxazolyl)-2-methyl-4-(methylsulfonyl) phenyl](5-hydroxy-1-methyl-1H-pyrazol-4-yl) methanone}. Subsequently, HPPD-inhibitors were tested individually with PSII-inhibitors atrazine, or bentazon [3-(1-methylethyl)-(1H)-2,1,3-benzothiadiazin-4(3H)-one2,2-dioxide], or alone in field experiments on all three CYP genotypic classes; hybrids homozygous for mutant CYP alleles (cypcyp), hybrids homozygous for functional alleles (CYPCYP), and heterozygous hybrids (CYPcyp). Leaf bleaching within 1 wk of herbicide application increased when a PSII-inhibitor was combined with an HPPD-inhibitor; however, the relatively low level of injury was short-lived. Tank mixing atrazine to mesotrione, tembotrione, or topramezone in sweet corn did not increase risk of yield loss compared to HPPD-inhibitor applied alone. The synergistic effect on weed control between certain PSII-and HPPD-inhibitor combinations reported previously does not hold true regarding sweet corn sensitivity to these herbicides. Among three HPPD-inhibitors tested in sweet corn, topramezone was the safest, regardless of PSII combination. Mutant CYP alleles, namely CYPcyp and cypcyp hybrids, are the main cause of sweet corn sensitivity to mesotrione, tembotrione, and other CYP-metabolized herbicides; therefore, breeding efforts to eliminate mutant CYP alleles should remain a high priority.

Maize dwarf mosaic (MDM) stunts corn growth, delays development, and is the most prevalent viral disease of sweet corn grown in many regions of North America and Europe. Although some weeds escape control in most sweet corn fields, the extent to which MDM influences the weed suppressive ability of the crop is unknown. Field studies were conducted over a 3-yr period to characterize the influence of variable MDM incidence in sweet corn on growth, fecundity, and germinability of wild-proso millet, a common weed in the crop. Treatments included five levels of MDM incidence (0, 25, 50, 75, and 100% of plants infected) in two MDM-susceptible hybrids differing in weed suppressive ability. Previous research showed that hybrid ‘Legacy’ had greater weed suppressive ability than ‘Sugar Buns’. Wild-proso millet biomass and fecundity depended largely on the hybrid in which the weed was growing. Wild-proso millet growing in Sugar Buns weighed 45 to 117% more than wild-proso millet in Legacy. Incidence of MDM in sweet corn affected wild-proso millet biomass and fecundity, but only under high weed population densities. When wild-proso millet was observed at 122 plants m−2, weed biomass increased 9 g m−2 for each additional 10% incidence of MDM of sweet corn. Weed suppressive ability of the competitive and less competitive hybrids were influenced to the same extent by MDM. Coupled with a lack of resistance to MDM in two-thirds of commercial sweet corn hybrids, the disease could be an additional factor perpetuating weed growth and fecundity in sweet corn, particularly in fields with high population densities of wild-proso millet.

Maize dwarf mosaic (MDM) and weed interference are two economically important stresses to sweet corn; however, a fundamental understanding of the extent to which the crop is affected by combinations of these stresses is lacking. The objective of this study was to quantify the extent to which MDM incidence and weed interference influence the sweet corn canopy. phenological development, and yield. In field research, five levels of MDM incidence (0, 25%, 50%, 75%, and 100% of the plant population) were established in two sweet corn hybrids that also were grown in the presence or absence of wild-proso millet. During the vegetative phase of crop growth, the crop's ability to tolerate these multiple stresses was largely additive. For instance, incidence of MDM decreased crop growth and delayed development by as much as five days, and wild-proso millet added to those detrimental effects by an extent that was determined by the severity of weed interference. In contrast during the reproductive phase, MDM incidence and weed interference interacted in their effect on the crop. Moreover, differences in hybrid responses to the multiple stresses indicated that the benefit of improved crop tolerance to weed interference was not lost when the crop is infected with MDM. Use of hybrids with high levels of MDM resistance and improved competitive ability with weeds reduces the risk of losses from MDM and weed interference, two commonly occurring stresses in sweet corn. Published by Elsevier B.V.

HomePlant DiseaseVol. 95, No. 12Observations from a Quarter Century of Evaluating Reactions of Sweet Corn Hybrids in Disease Nurseries PreviousNext FeatureObservations from a Quarter Century of Evaluating Reactions of Sweet Corn Hybrids in Disease NurseriesJerald K. Pataky, Martin M. Williams II, John M. Headrick, Claude Nankam, Lindsey J. du Toit, and Phillip M. MichenerJerald K. PatakyDr. Pataky's address is: University of Illinois, Department of Crop Sciences, Urbana, IL 61801; E-mail: E-mail Address: [email protected]Search for more papers by this author, Martin M. Williams IISearch for more papers by this author, John M. HeadrickSearch for more papers by this author, Claude NankamSearch for more papers by this author, Lindsey J. du ToitSearch for more papers by this author, and Phillip M. MichenerSearch for more papers by this authorAffiliationsAuthors and Affiliations Jerald K. Pataky , University of Illinois, Department of Crop Sciences, Urbana Martin M. Williams II , USDA-ARS, Global Change and Photosynthesis Research Unit, University of Illinois, Urbana John M. Headrick , Monsanto Company, Seminis Vegetable Seeds, St. Louis, MO Claude Nankam , World Vision Internationalm Malawi Lindsey J. du Toit , Washington State University, Department of Pland Pathology, Mount vernon Phillip M. Michener , Terai Seeds, Greenville, MS Published Online:10 Nov 2011https://doi.org/10.1094/PDIS-03-11-0236AboutSectionsPDF ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InRedditEmailWechat DetailsFiguresLiterature CitedRelated Vol. 95, No. 12 December 2011SubscribeISSN:0191-2917e-ISSN:1943-7692 Metrics Article History Issue Date: 10 Nov 2011Published: 10 Nov 2011 Pages: 1492-1506 Information© 2011 The American Phytopathological SocietyPDF downloadCited byClavibacter nebraskensis causing Goss's wilt of maize: Five decades of detaining the enemy in the New World18 September 2022 | Molecular Plant Pathology, Vol. 24, No. 7Susceptibility of Almond (Prunus dulcis) Cultivars to Twig Canker and Shoot Blight Caused by Diaporthe amygdaliFrancisco Beluzán, Xavier Miarnau, Laura Torguet, Lourdes Zazurca, Paloma Abad-Campos, Jordi Luque, and Josep Armengol13 June 2022 | Plant Disease, Vol. 106, No. 7Historical Trends in Sweet Corn Plant Density Tolerance Using Era Hybrids (1930–2010s)22 September 2021 | Frontiers in Plant Science, Vol. 12Optimum plant density for crowding stress tolerant processing sweet corn26 September 2019 | PLOS ONE, Vol. 14, No. 9Variability in Susceptibility to Anthracnose in the World Collection of Olive Cultivars of Cordoba (Spain)6 November 2017 | Frontiers in Plant Science, Vol. 8Alternatives to Atrazine for Weed Management in Processing Sweet Corn20 January 2017 | Weed Science, Vol. 64, No. 3Identifying Crowding Stress‐Tolerant Hybrids in Processing Sweet Corn1 September 2015 | Agronomy Journal, Vol. 107, No. 5Relative Susceptibility of New Olive Cultivars to Spilocaea oleagina, Colletotrichum acutatum, and Pseudocercospora cladosporioidesJ. Moral, M. Alsalimiya, L. F. Roca, C. M. Díez, L. León, R. de la Rosa, D. Barranco, L. Rallo, and A. Trapero6 August 2014 | Plant Disease, Vol. 99, No. 1Maize Dwarf Mosaic Can Reduce Weed Suppressive Ability of Sweet Corn20 January 2017 | Weed Science, Vol. 60, No. 4Interactions between maize dwarf mosaic and weed interference on sweet cornField Crops Research, Vol. 128

Common rust, northern leaf blight (NLB), Stewart's bacterial wilt, maize dwarf mosaic (MDM), and southern leaf blight (SLB) can reduce yields of susceptible and moderately susceptible sweet corn hybrids. Disease management can be improved if reactions of hybrids are known. Resistance and susceptibility are the two extremes of a continuum of host reactions to diseases. Resistance is a measure of the ability of the host to reduce the growth, reproduction and/or disease-producing abilities of the pathogen, thus resulting in less severe symptoms of disease. Major genes for resistance, such as Rp , Ht, or Mdm1, can prevent or substantially limit disease development if specific virulence is not present in pathogen populations. Hybrids with major gene resistance usually are identified from specific phenotypes. Major gene resistance may be ineffective when specific virulence occurs. In the absence of effective major gene resistance, disease reactions often range from partially resistant to susceptible. Hybrids can be grouped into broad classes such as: resistant (R), moderately resistant (MR), moderate (M), moderately susceptible (MS), and susceptible (S) based on severity of disease symptoms. This procedure produces statistically "overlapping" groups without clear-cut differences between classes (e.g., the hybrid with least severe symptoms in the MR class does not differ significantly from the hybrid with the most severe symptoms in the R class). Nevertheless, a consistent response over several trials produces a reasonable estimate of the disease reaction of a hybrid relative to the response of other hybrids. These reactions can be used to assess the potential for diseases to become severe and affect yield (2). This report summarizes the reactions of 247 sweet corn hybrids to common rust, NLB, Stewart's wilt, MDM, and SLB based on performance in the 2000 University of Illinois sweet corn disease nursery.

Sensitivity to certain P450-metabolized herbicides in corn ( Zea mays L.) is largely conditioned by a single cytochrome P450 (CYP) gene. Little to no research has been done to evaluate the effect of CYP genotype on sweet corn yield. Yield of 23 sweet corn hybrids of known CYP genotype was evaluated in 2007, 2008, and 2009 following postemergence applications of mesotrione, an hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor, or nicosulfuron, an acetolactate synthase (ALS) inhibitor, at two growth stages. Mesotrione and nicosulfuron were evaluated in separate experiments. Treatments included herbicide application during the V3 to V5 or V5 to V7 growth stages and a nontreated control. Crop injury, measured 7 d after treatment (DAT), ranged from 0 to 87% for mesotrione and 0 to 54% for nicosulfuron among CYP genotypes. Injury from both mesotrione and nicosulfuron was most severe following application during V3 to V5 growth stages on hybrids with mutant (i.e., nonfunctional) cyp alleles. Only hybrids homozygous for mutant cyp alleles (i.e., cypcyp ) suffered yield losses from mesotrione, ranging from 9 to 40%. These hybrids were not evaluated for nicosulfuron because applications of ALS-inhibiting herbicides kill cypcyp hybrids. Nicosulfuron reduced the yield of CYPcyp hybrids only; whereas mesotrione did not. Yield losses from nicosulfuron ranged from 9 to 35% among CYPcyp hybrids and were associated with moderate to severe loss of kernel rows (i.e., ear pinching). Yield of CYPCYP hybrids was not affected by mesotrione or nicosulfuron.

Maize dwarf mosaic (MDM), caused by Maize dwarf mosaic virus (MDMV) and Sugarcane mosaic virus (SCMV), is an economically important viral disease of sweet corn (Zea mays). MDM is known to increase the severity of fungal root rots and southern corn leaf blight (SCLB). The effect of infection with MDMV-A and SCMV on eight foliar diseases was evaluated on 32 sweet corn hybrids (27 MDM-susceptible hybrids and five MDM-resistant hybrids) in 2007, 2008, and 2009. Virus infection substantially increased the severity of five diseases, including: SCLB, northern corn leaf spot (NCLS), gray leaf spot (GLS), Diplodia leaf streak (DLS), and eyespot. Among MDM-susceptible hybrids, mean severity of SCLB, NCLS, GLS, DLS, and eyespot on virus-infected plants was typically double that of plants that were asymptomatic of viral infection. Three diseases were not substantially increased by MDM, including: common rust, northern corn leaf blight (NCLB), and Stewart's wilt. Virus infection appeared to affect the severity of diseases caused by necrotrophic foliar fungi that colonize mesophyll tissue. MDM did not appear to substantially affect the severity of diseases caused by pathogens that form haustoria or invade the vascular system. The extent to which SCLB severity is increased by MDM in terms of changes in level of host resistance also was determined. For MDM-susceptible hybrids, reactions to SCLB ranged from resistant to moderately susceptible in MDM-free treatments, but each of these hybrids was classified as moderately susceptible to susceptible when infected with MDMV-A and/or SCMV. The results of this experiment demonstrate the importance of breeding for MDM resistance, not only to control this important viral disease of sweet corn, but also to lower the potential for detrimental effects from several other foliar diseases that often are of minor importance on sweet corn in the absence of MDM.

Many sweet corn (Zea mays) hybrids commercially available today have higher levels of resistance to Stewart's disease (caused by Pantoea stewartii subsp. stewartii) than the cultivars from which Stevens developed the first forecast of this disease in the 1930s. Incorporating levels of host resistance into forecasts of the seedling wilt phase of Stewart's disease (i.e., Stewart's wilt) could improve control decisions for sweet corn which are made prior to planting. Incidence of systemic infection of seedlings was assessed on 27 sweet corn hybrids with a range of reactions to P. stewartii. In total, 741 observations were collected from 1998 to 2009 in 79 field trials at 15 locations throughout Illinois and one each in Kentucky and Delaware. Relative frequency distributions of the incidence of systemic Stewart's wilt were developed for combinations of hybrids with different levels of resistance and ranges of winter temperature from Stewart's wilt forecasts. The probability of exceeding thresholds of 1 or 5% incidence that warrant the use of seed-treatment insecticides on sweet corn grown for fresh market or processing, respectively, was determined from these frequency distributions. Levels of host resistance affected the incidence of systemic seedling wilt within ranges of winter temperatures used by Stewart's wilt forecasts. For moderate and resistant hybrids, frequency distributions of Stewart's wilt incidence and mean incidence ranging from 0.7 to 1.8% did not differ among three winter temperature ranges above -2.8°C. Conversely, distributions of Stewart's wilt incidence on susceptible hybrids differed among each of the four ranges of winter temperature from the Stevens-Boewe forecast (i.e., >0.6, -1.1 to 0.6, -2.8 to -1.1, and <-2.8°C), with mean incidence ranging from 0.5 to 8.5%. Occurrence of Stewart's wilt also differed among trials varying in number of winter months above -4.4°C, the criterion used by the Iowa State forecast of this disease. Levels of host resistance to P. stewartii also affected the occurrence of Stewart's wilt as predicted by the Iowa State method. The probability of exceeding economic thresholds of 1 or 5% incidence of systemic Stewart's wilt depended on levels of host resistance and winter temperature. Stewart's wilt is unlikely to exceed economic thresholds when the mean winter temperature is below -4.4°C. When mean winter temperature was above -2.8°C, the probability of exceeding 1% incidence of systemic Stewart's wilt was 0.59 for susceptible sweet corn hybrids and 0.28 for moderate and resistant hybrids. When mean winter temperature was below -2.8°C, the probability of exceeding 1% incidence of systemic Stewart's wilt was 0.22 for susceptible hybrids and 0.04 for moderate or resistant sweet corn hybrids. The probability of exceeding 5% incidence was less than 0.1, except when the mean winter temperature was above -2.8°C and susceptible hybrids were grown.

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 amongCYPCYP,CYPcyp, andcypcyphybrids. 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 exclusivelycypcyporCYPcyp. The safener isoxadifen added to the tembotrione product greatly reduced occurrence of injury to theCYPcypgenotypic class but not to thecypcyphybrids. 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.

Knowledge of cultivar-specific information on crop tolerance, the ability of the crop to endure competitive stress from weeds, has garnered recent interest in organic crop production. Twenty-five commercial sweet corn hybrids from nine seed companies were grown in the presence and absence of wild-proso Millet (Panicum miliaceum L.) to 1) quantify tolerance in crop growth and yield to weed interference; 2) determine associations between tolerance in crop growth and yield; and 3) identify hybrids differing in tolerance to weed interference. Despite large differences in canopy architecture among hybrids, crop height and leaf uprightness were minimally affected by weed interference. in contrast, wild-proso millet interference reduced ear number 11% to 98% and ear mass 24% to 82% depending on the hybrid. The ability of a hybrid to make small growth adjustments in the presence of wild-proso millet appeared to have no relationship to yield tolerance. The least competitive hybrids were 'ACX1413', 'Optimum', 'Quickie', 'Spring Treat', and 'Sugar Buns'. The most competitive hybrids were 'Code128', 'Coho','El Toro', 'EX 8716622', and 'Legacy'. Although some exceptions were observed, in general, the longer-maturity processing hybrids were more competitive with wild-proso millet than the earlier-maturing fresh market hybrids.

Southern rust, caused by Puccinia polysora Underw., occurs frequently on corn (Zea mays) grown in subtropical or tropical regions. When conditions are favorable, southern rust also occurs in temperate climates of the central and southern United States although the fungus does not survive on corn crop residue and must be introduced to temperate regions each growing season. Several single, dominant, resistance genes, designated as Rpp genes, convey hypersensitive, chlorotic fleck reactions when challenged with avirulent isolates of P. polysora (1). Rpp resistance prevents or limits the formation of uredinia. The Rpp9 gene has been used successfully in North America in the past 20 years to control southern rust even though the gene has been ineffective in other parts of the world (e.g., Africa and Hawaii) because of the prevalence of virulent races. During the past 3 years, Rpp9 virulence has occurred in the western hemisphere (e.g., Brazil, Mexico, Nebraska, and Texas), but prior to 2008, uredinia were not observed east of the Mississippi River on corn with the Rpp9 gene. A few uredinia were observed on corn with the Rpp9 gene in eastern Nebraska in 2006 and near Victoria, TX in 2007 (W. Dolezal, personal observation). In July of 2008, a virulent isolate of P. polysora was confirmed from Grady County, GA on corn lines with the Rpp9 gene including the original source of this resistance gene, Boesman yellow flint, which is PI 186208 (3). In August of 2008, isolates of P. polysora were collected from severely infected corn hybrids with Rpp9 grown in Macon County, GA. Rust samples from hybrids without Rpp genes also were collected in Burke County, GA where Rpp-resistant corn was asymptomatic. In greenhouse trials, corn lines with and without the Rpp9 gene were inoculated with urediniospores from collections from Burke and Macon counties and Illinois. Rust infection types (1) were scored 18 to 25 days after inoculation. The Macon County isolate produced type 1 and 2 infections (small uredinia surrounded by necrotic or chlorotic tissue) on Oh43Rpp9 and W64aRpp9 and type 4 infections (large, sporulating uredinia) on two versions of a commercial hybrid with and without the Rpp9 gene and on Va59 (which carries an Rpp gene different from Rpp9). The Burke County isolate and an isolate from Illinois collected in 2001 produced type 0 infections (chlorotic flecks) on all of these lines except the non-Rpp version of the commercial hybrid which had a type 4 reaction. To our knowledge, Rpp9-virulent isolates of P. polysora have not been reported from the continental United States for nearly 50 years. In the late 1950s and early 1960s, A. L. Robert (2) collected isolates of P. polysora from throughout the world and observed multiple races on a set of host differentials that is no longer available. A. L. Robert's collection included an isolate from Georgia that was virulent on PI 186208. Commercial hybrids containing the Rpp9 gene may continue to be resistant throughout most of North America if previously common Rpp9-avirulent isolates of P. polysora are prevalent, but those hybrids should be carefully monitored for infection by newly introduced Rpp9-virulent isolates. References: (1) A. L. Hooker. Page 207 in: The Cereal Rusts. Vol. II. Academic Press, San Diego, 1985. (2) A. L. Robert. Phytopathology 52:1010, 1962. (3) A. J. Ullstrup. Phytopathology 55:425, 1965.

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 F 2 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 F 2 progeny from crosses of inbreds with Cr1 were also tested. Based on segregation of progeny from testcrosses with Cr1 and Cr2 and the F 2 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.

Univariate analyses fail to account for covariance among phenomorphological traits implicated in crop competitive ability. A more complete analysis of cultivar–weed interactions would reduce a number of important traits to a few underlying principal factors responsible for sweet corn competitiveness. Twenty-three commercial sweet corn hybrids from nine seed companies were grown in the presence and absence of wild-proso millet to (1) quantify the extent to which phenomorphological traits vary in sweet corn, (2) identify underlying principal factors that describe variation in crop canopy development, and (3) determine functional relationships between crop canopy factors and competitive ability. A principal component factor analysis revealed that 7 of the 18 weed-free crop traits measured at silking loaded highly (0.65 to 0.90) into the first factor, including plant height, shoot biomass, per plant leaf area, leaf area index, and intercepted light, as well as thermal time from emergence to silking and emergence to maturity. All seven traits were highly correlated (0.38 to 0.93) and were interpreted as a “late canopy and maturity” factor. Another five traits formed two additional principal factors that were interpreted as an early “seedling quality” factor (e.g., kernel mass, seedling vigor, and height at two-leaf stage) and a mid-season “canopy closure” factor (e.g., leaf area index and intercepted photosynthetically active radiation at six-leaf stage). Relationships between principal factors and competitive abilities were quantified using least-squares linear regression. Cultivars with greater loadings in the late canopy and maturity and canopy closure factors were more competitive with wild-proso millet. In contrast, crop competitive ability declined with cultivars that loaded highly into the seedling quality factor. The analyses showed that sweet corn's ability to endure weed interference and suppress weed fitness relates uniquely to three underlying principal factors that capture crop canopy development around emergence and near canopy closure and during the reproductive phase.

Over the last two decades, sweet corn injury from postemergence herbicides has resulted in routine screening of combinations of new and existing hybrids and herbicides. Sensitivity of sweet corn to several cytochrome P450-metabolized herbicides is simply inherited and has a common genetic basis, a single P450 locus that may account for a large amount of the variation in sweet corn injury commonly observed among screening trials. Using data from 13 hybrid-herbicide screening trials, the objective of this work was to determine the extent to which injury from P450-metabolized herbicides was associated with the genotypes of hybrids at a locus affecting herbicide sensitivity. Of the 703 hybrids evaluated in the University of Illinois sweet corn hybrid nurseries from 2002 to 2007, previous work showed that a total of 104, 70, and nine of the hybrids were known to be homozygous-tolerant, heterozygous, or homozygous-sensitive, respectively, for an allele affecting herbicide response. Nurseries from 2002 to 2007 included six trials with mesotrione, three trials with nicosulfuron, and one trial each with foramsulfuron, tembotrione, halosulfuron, and carfentrazone. When means of hybrids in genotypic classes were compared, homozygous-sensitive hybrids were consistently injured more severely than homozygous-tolerant and heterozygous hybrids. When environmental conditions favored crop injury, heterozygous hybrids had an intermediate response that was closer to homozygous-tolerant hybrids than homozygous-sensitive hybrids. These data are further evidence that the probability of injury from several P450-metabolized herbicides, including mesotrione, nicosulfuron, foramsulfuron, tembotrione, halosulfuron, and carfentrazone, is highest in homozygous-sensitive hybrids and least in homozygous-tolerant hybrids and that variability of responses among sweet corn hybrids to these P450-metabolized herbicides can be explained largely by the genotype of a hybrid at a single locus.

Nicosulfuron, mesotrione, dicamba plus diflufenzopyr, and carfentrazone are postemergence herbicides from different chemical families with different modes of action. An association between the sensitivity of sweet corn to these herbicides was observed when 143 F 3 : 4 families (F 4 plants) derived from of a cross between Cr1 (sensitive inbred) and Cr2 (tolerant inbred) were evaluated in greenhouse trials. The ratio of tolerant : segregating : sensitive families was not significantly different from a 3 : 2 : 3 ratio, which would be expected if a single gene conditioned herbicide response. Families cosegregated for responses to these herbicides. In field studies with 60 F 3 : 5 families in 2005 and 120 F 3 : 5 families in 2007, responses to these herbicides and foramsulfuron and primisulfuron were associated. Responses to bentazon in field trials were similar to the aforementioned herbicides for tolerant families, but differences were noted for families that were sensitive or segregated for responses to nicosulfuron, foramsulfuron, primisulfuron, mesotrione, dicamba plus diflufenzopyr, and carfentrazone. The gene(s) affecting herbicide sensitivity in Cr1 maps to the same region of chromosome 5S as a previously sequenced cytochrome P450 gene, where alleles previously designated nsf1 and ben1 were associated with sensitivity to nicosulfuron and bentazon and appear to be the result of a 392–base-pair insertion mutation. This work supports the hypothesis that a single recessive gene or closely linked genes in the sweet corn inbred Cr1 condition sensitivity to multiple cytochrome P450 enzyme-metabolized herbicides.