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  • Author or Editor: Jerald K. Pataky x
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Host resistance is the most efficient way to control common smut (Ustilago maydis) in sweet corn, but resistance to U. maydis is not understood well. All meristematic tissues are susceptible, but infection is localized. Ear galls result from infection of ovaries. Infection and resistance can be affected by plant morphology. For example, ovaries are protected from U. maydis infection when an abscission zone forms at the base of the silk 6–24 h after a pollen tube reaches an ovary. The objective of this study was to determine if the rate of silk abscission differed between two related sweet corn hybrids that differed in susceptibility to smut infection of ears. The two hybrids, Green Giant Code 3 (GG3) and Green Giant Code 46 (GG46), were evaluated for the occurrence of infected ears in 58 paired plots at four locations near Le Sueur, MN, from 1993 to 1999. The rate of silk abscission in the two hybrids was evaluated in two field trials in Urbana, IL, in 2002 and 2004. Incidence and severity of ear smut were significantly (P < 0.05) greater and about twice as much on GG3 than on GG46. Silk abscission was more rapid on GG46 than on GG3. Although this association does not prove that decreased susceptibility of GG46 to ear infection is due to silk abscission, it is a logical basis from which to hypothesize that silk dynamics and other aspects of maize floral biology play important roles in resistance to ear infection by minimizing the time period that all ovaries on an ear are exposed to infection by U. maydis. This hypothesis is discussed in relation to the results of this and other research.

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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.

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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.

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Ten cycles of simple mass selection for increased field emergence and kernel weight in a population of shrunken2 (sh2) maize affected various kernel and seedling traits. Ten of 29 variables measured were intercorrelated and were included in the first principal factor of a principal component, factor analysis. The eight variables in factor 1 that increased with cycles of selection were: emergence and kernel weight (the two selection criteria) plant height 41 days after planting (a measure of seedling vigor), uniformity of stand, total starch content per kernel total carbohydrate content per kernel, concentration of starch, and starch content per kernel. The two variables in factor 1 that decreased were: conductivity of electrolytes that leached from imbibing seeds and symptomatic infection of kernels by fungi. Factor 1 was a “seed and seedling quality” factor. The other 19 variables formed five principal factors that primarily were “sugar,” “pericarp,” and “asymptomatic fungal infection” factors. These five factors and the variables from which they were formed, were not affected by selection. These results suggest that seed and seedling quality factors can be improved by selection in a sh2 population without affecting sweetness or tenderness. These results also suggest that although selection for increased emergence and kernel weight lowered the incidence of symptomatic infection by fungi, the population was not improved specifically for resistance to Fusarium moniliforme Sheldon.

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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, F2:3 (S1:2) and F3:4 (S2:3) 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, F2:3, and F3:4 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.

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Resistance to Puccinia sorghi Schwein. based on the Rp1-D gene has been used successfully in North America for the past 15 years to control common rust on sweet corn (Zea mays L.). The objective of this preliminary research was to examine rust reactions of Rp-hybrids grown for processing in the midwestern United States against biotypes of P. sorghi virulent against Rp1-D. In Sept. 1999, isolates of P. sorghi virulent on corn with the Rp1-D gene were collected throughout the midwestern United States. Rust reactions of 41 Rp-resistant, processing sweet corn hybrids and nine non-Rp hybrids were evaluated during the 1999-2000 season in Argentina, Hawaii, Mexico, and South Africa, where populations of P. sorghi are virulent against Rp1-D. Sporulating uredinia were observed on all hybrids in all locations. Although rust reactions varied among locations, mean standardized scores of nine non-Rp hybrids that were included in the trial as controls ranked nearly the same as in previous trials. Thirteen hybrids with standardized scores above 0.25 were more susceptible than the hybrid with the lowest mean rust rating, `Green Giant Code 27'. Thirty-two hybrids were intermediate in reaction to P. sorghi virulent against Rp1-D. Reactions were moderately resistant for nine hybrids with mean standardized scores below -0.50, including two moderately resistant, non-Rp hybrids (`GG Code 27' and `GG Code 6') that were included as controls. Additional trials are necessary to confirm reactions of these hybrids. If the Rp-hybrids that were moderately susceptible or susceptible in this trial are infected by P. sorghi virulent against Rp1-D, secondary inoculum will be abundant and infection will be severe if the weather is wet.

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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.

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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.

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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).

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