Influence of Host Resistance on Stewart's Wilt Forecasts and Probability of Exceeding Thresholds for Use of Seed-Treatment Insecticides on Sweet Corn.

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.

Increased Severity of Foliar Diseases of Sweet Corn Infected with Maize Dwarf Mosaic and Sugarcane Mosaic Viruses.

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.

Selection for quantitative trait loci associated with resistance to Stewart's wilt in sweet corn.

The objectives of this research were to identify quantitative trait loci (QTL) for Stewart's wilt resistance from a mapping population derived from a sweet corn hybrid that is highly resistant to Pantoea stewartii and to determine if marker-based selection for those QTL could substantially improve Stewart's wilt resistance in a population derived from a cross of resistant lines and a highly susceptible sweet corn inbred. Three significant QTL for Stewart's wilt resistance on chromosomes 2 (bin 2.03), 5 (bin 5.03), and 6 (bin 6.06/6.07) explained 31% of the genetic variance in a population of 110 F(3:4) families derived from the sweet corn hybrid Bonus. The three QTL appeared to be additive in their effects on Stewart's wilt ratings. Based on means of families that were either homozygous or heterozygous for marker alleles associated with the resistance QTL, the QTL on chromosomes 2 and 6 appeared to have dominant or partially dominant gene action, while the QTL on chromosome 5 appeared to be recessive. A population of 422 BC(2)S(2) families was derived from crosses of a sweet corn inbred highly susceptible to Stewart's wilt, Green Giant Code 88 (GG88), and plants from two F(3:4) families (12465 and 12467) from the Bonus mapping population that were homozygous for marker alleles associated with Stewart's wilt resistance at the three QTL. Mean Stewart's wilt ratings for BC(2)S(2) families were significantly (P < 0.05) lower for families that were homozygous for the bnlg1902 marker allele (bin 5.03) from resistant lines 12465 or 12467 than for families that were heterozygous at this marker locus or homozygous for the bnlg1902 marker allele from GG88. Resistance associated with this QTL was expressed only if F(3:5) or BC(2)S(2) families were homozygous for marker alleles associated with the resistant inbred parent (P(1)). Marker alleles identified in the F(3:5) mapping population that were in proximity to the resistance QTL on chromosomes 2 and 6 were not polymorphic in crosses of GG88 with 12465 and 12467. Selection for other polymorphic marker loci adjacent to these two regions did not improve Stewart's wilt resistance of BC(2)S(2) families.

First Report of Phoma terrestris Causing Red Root Rot on Sweet Corn (Zea mays) in North Carolina.

Red root rot, caused by Phoma terrestris E. M. Hansen, caused premature senescence and yield reductions to fresh-market sweet corn in Hyde County, North Carolina in July 2006. Foliar symptoms developed over a period of 5 to 8 days approximately 1 to 2 weeks after anthesis and included desiccation of leaves and poor development of ears. By 3 weeks after pollination, when the sweet corn was harvested, crowns and the first aboveground internode of affected plants were rotted and reddish colored, but roots appeared normal. The root mass of affected plants tended to be greater than that of unaffected plants. Incidence of symptomatic plants was greater than 30% in some fields and was lower on crops planted and harvested early. Symptomatic and asymptomatic plants were adjacent in affected fields. Diseased plants were more common in fields of sweet corn that followed soybean (Glycine max) or a double-crop of onions (Allium cepa) than in fields that followed corn. Incidence of symptomatic plants also differed among adjacent plantings of different sweet corn hybrids. Hybrids '173A', '182A', '378a', and 'XTH1178' had a high incidence of symptomatic plants and '372A', '278A', '8101', and '8102' were less affected. Samples of symptomatic plants of the hybrid '182A' were examined at the North Carolina Plant Disease and Insect Clinic during August. Olivaceous black pycnidia with long setae around the ostioles were imbedded in the stalk near the first node aboveground. Numerous conidia (1.8 to 2.3 × 4.5 to 5.5 µm) were released in cirri from pycnidia. When cultured on potato dextrose agar (PDA), the fungus produced a red pigment and intercalary and terminal chlamydospores. Pathogenicity was demonstrated in the greenhouse by transplanting corn seedlings or direct-seeding corn into pots of soil infested with plates of PDA containing chlamydospores and hyphae. A suspension of chlamydospores and hyphae also was injected into the stems of plants 28 days after transplanting. Five replicates of the pathogenicity experiments were repeated twice with noninoculated controls. After 8 weeks, P. terrestris was recovered from the roots of all inoculated plants. Soil inoculation resulted in necrotic root tissue in approximately 25% of inoculated plants. Approximately 90% of inoculated plants had discolored crowns that resembled symptoms from field infected plants. Stem inoculations resulted in necrosis extending 2 to 5 cm from the point of injection and resulted in shoot death of 40% of inoculated plants that resulted in the development of an adventitious shoot. Red root rot was prevalent on field corn in the Delmarva Peninsula throughout the late 1980s and 1990s (1). To our knowledge, this is the first report of this disease causing damage to sweet corn in North Carolina. Foliar symptoms and discoloration of crowns of diseased sweet corn plants were similar to previously described symptoms of red root rot on field corn (2), however, roots of affected sweet corn plants were not substantially rotted and did not have a symptomatic reddish pink or dark carmine color, presumably because sweet corn is harvested prior to the development of root symptoms. References: (1) K. W. Campbell et al. Plant Dis. 75:1186, 1991. (2) D. G. White, ed. Compendium of Corn Diseases. The American Phytopathological Society, St Paul, MN, 1999.

Development of Gibberella Ear Rot on Processing Sweet Corn Hybrids Over an Extended Period of Harvest.

Gibberella ear rot, caused by Gibberella zeae, has increased in prevalence recently on lateseason processing sweet corn grown in North America. Little information is available about the development of Gibberella ear rot on processing sweet corn hybrids over extended periods of harvest. In five trials from 2003 to 2005, 12 processing sweet corn hybrids were inoculated with G. zeae and evaluated for severity of Gibberella ear rot on sequential harvest dates from 19 to 27 days after midsilk. Ear rot severity was assessed using a rating scale based on the percentage of kernels with visible symptoms of G. zeae colonization including kernel rot and mycelial growth. Severity ranged from 1.6 to 47.8% over the five trials. None of the hybrids was highly resistant to Gibberella ear rot, although some appeared to be less susceptible. Gibberella ear rot was less severe on three hybrids (GH 2690, GG 147, and Sprint) and more severe on three hybrids (GG 42, GG 145, and Jubilee). Other hybrids had moderate levels of ear rot or responses that varied among years. The relative response of hybrids did not change substantially during the extended period of harvest; however, the rate at which Gibberella ear rot developed on hybrids differed in 2003 and 2005 as reflected by a significant hybrid by harvest interaction. The interaction was primarily the result of Gibberella ear rot developing more severely on susceptible hybrids than on the less susceptible hybrids. The difference in Gibberella development could be exploited to limit losses due to this disease under certain circumstances. If a sweet corn processor had several fields ready to harvest at the same time, and some fields were planted with hybrids that are more susceptible while other fields were planted with hybrids that are less susceptible, losses due to Gibberella ear rot might be minimized by harvesting the most susceptible hybrids first. Other hybrids that might be best suited for early or late harvest can be identified from Gibberella ear rot ratings 28 days after silk channel inoculation at the midsilk growth stage.

Resistance Conferred by the Ht1 Gene in Sweet Corn Infected by Mixtures of Virulent and Avirulent Exserohilum turcicum.

The Ht1 gene conveys a chlorotic-lesion resistant reaction in corn infected by avirulent races of Exserohilum turcicum, the causal agent of northern corn leaf blight (NCLB). The widespread deployment of the Ht1 gene in field corn grown in North America since the 1960s resulted in an increased frequency of E. turcicum race 1, which is virulent against the Ht1 gene. The objective of this study was to assess the value of resistance conveyed by the Ht1 gene when initial inoculum consisted of different ratios of virulent and avirulent E. turcicum. Forty-two sweet corn hybrids with the Ht1 gene and 42 sweet corn hybrids without Ht1 were grown in five trials each in 2003 and 2004. In each trial, plants were inoculated with culture suspensions consisting of different percentages of E. turcicum race 0 and race 1, including: 100:0, 90:10, 75:25, 50:50, and 0:100. Severity of NCLB was rated visually from 0 to 100% leaf area infected when plants were about 3 to 4 weeks past the mid-silk growth stage. The Ht1 gene reduced severity of NCLB by as much as one-third when virulent isolates comprised 25% or less of the initial inoculum. Reduction in NCLB severity due to the Ht1 gene was more substantial on hybrids with susceptible backgrounds than on those with general resistance. When virulent isolates comprised 50% of the initial inoculum, NCLB severity was similar for hybrids with and without the Ht1 gene if hybrids had equivalent levels of general resistance (measured as NCLB severity from trials inoculated entirely with race 1). To accurately classify NCLB reactions of maize lines relative to their most probable performance in the United States, inoculum should consist of at least 50% E. turcicum race 1.

Population densities of corn flea beetle (Coleoptera: Chrysomelidae) and incidence of Stewart's wilt in sweet corn.

To quantify populations of the corn flea beetle, Chaetocnema pulicaria Melsheimer (Coleoptera: Chrysomelidae), and refine estimates of a threshold for its control to prevent Stewart's wilt caused by Erwinia stewartii, sequential plantings of 'Jubilee' sweet corn were made at 2-wk intervals from April or May through August or September 2001 and 2002 at four locations from southern to northern Illinois: Simpson, Brownstown, Champaign, and Mendota. Densities of C. pulicaria and incidence of Stewart's wilt were monitored weekly. At Mendota, where C. pulicaria populations were decimated by cold temperatures during winter 2000-2001, densities reached 33.3 beetles per 15-cm yellow sticky trap per day by September 2002, after a mild 2001-2002 winter. Maximum incidence of Stewart's wilt in single plots at Simpson, Brownstown, Champaign, and Mendota was 22, 36, 39, and 2%, respectively, in 2001, and 33, 47, 99, and 87%, respectively, in 2002. In 24 plots where beetle densities were < or =2 per trap per day, Stewart's wilt incidence was <5% in 20 plots. We propose that two corn flea beetles per trap per day be used as a threshold for insecticide application to seedlings to control C. pulicaria and minimize subsequent incidence of Stewart's wilt in processing sweet corn. Enzyme-linked immunosorbent assays indicated that E. stewartii incidence in C. pulicaria peaked at 67, 62, and 54%, respectively, at Simpson, Brownstown, and Champaign, in 2001, and at 71, 76, and 60%, respectively, in 2002. Further studies might allow the use of areawide or field-specific estimates of E. stewartii incidence in corn flea beetles for adjusting management decisions.

Frequency of the Ht1 Gene in Populations of Sweet Corn Selected for Resistance to Exserohilum turcicum Race 1.

ABSTRACT The possibility that the Ht1 gene or genes tightly linked to Ht1 convey general resistance to races of Exserohilum turcicum that are virulent against Ht1 (i.e., residual resistance) could be useful in sweet corn where the Ht1 gene is present in many commercial hybrids and breeding populations. The objective of this study was to determine if the frequency of the Ht1 gene changed in populations of sweet corn selected for general resistance to E. turcicum race 1, thus conveying residual resistance. Four populations were developed with theoretical initial frequencies of the Ht1 gene of 0, 0.25, 0.25, and 0.5. The populations were advanced by recurrent mass selection with parental control through four or five cycles of selection following inoculation with an Ht-virulent race of E. turcicum (i.e., race 1). Plants from each cycle of each population were evaluated for severity of northern corn leaf blight (NCLB) and chlorotic lesion reactions following inoculation in field and greenhouse trials with either race 0 or 1 of E. turcicum. Recurrent mass selection for general resistance to E. turcicum race 1 reduced the severity of NCLB in all four populations of sweet corn, although the change in the most susceptible population was minimal. Percent gain per cycle was 14.5, 12.3, 14, and 3.7% for populations I, II, III, and IV, respectively. The Ht1 gene did not convey levels of general resistance to E. turcicum race 1 that were substantial enough to be selected for in this population improvement program. There was no apparent selection advantage for resistance to E. turcicum race 1 in the populations that contained the Ht1 gene. The frequency of the Ht1 gene did not differ among cycles of selection within any of the populations in response to improved levels of general resistance to NCLB. The lack of change in frequency of Ht1 in these populations and the similarity in gain per cycle among populations with and without Ht1 lead us to conclude that the Ht1 gene itself did not have a residual effect on resistance.

Rates of Seed Treatment Insecticides and Control of Stewart's Wilt in Sweet Corn.

Neonicotinoid insecticides applied as seed treatments reduce the incidence of Stewart's wilt. The objectives of this study were to examine the efficacy of different rates of seed treatment insecticides to control Stewart's wilt on susceptible sweet corn hybrids and to compare the economic value of Stewart's wilt control in sweet corn grown for processing and fresh market. Clothianidin (Poncho), imidacloprid (Gaucho), and thiamethoxam (Cruiser) applied to seed at rates ranging from 0.125 to 1.25 mg a.i. per kernel were evaluated in 11 field trials in Illinois and Delaware from 2000 to 2003. Incidence of Stewart's wilt was significantly lower when seed was treated with insecticides than when plants were grown from nontreated seed in all but one trial. The level of control usually was between 50 and 90%. Small but statistically significant differences in incidence of systemically infected plants occurred among rates of insecticides in all trials except those in 2001. Usually, incidence of systemic Stewart's wilt was lower when higher rates of insecticides were applied; however, increasing the rate of insecticides from 0.125 mg a.i. to 1.25 mg a.i. per kernel had a relatively small effect on the level of Stewart's wilt control compared with the difference between treated and nontreated sweet corn seed. Based on a regression analysis, the lowest rates of the insecticides provided 64 to 72% control. The level of control increased about 1.85% with each additional 0.1 mg a.i. of insecticide per kernel from 0.125 mg a.i. to 1.25 mg a.i. Clothianidin provided an 8 or 9% higher level of control than thiamethoxam or imidacloprid at the same rate. Recommendations for application of seed treatment insecticides to processing and fresh market sweet corn differed somewhat due to substantial differences in the value of the crops. Based on estimated costs of $6 to $12 per 0.4 ha for the seed treatments, the economic break even point (i.e., cost of control = value from control) occurred in the range of 3 to 6% Stewart's wilt incidence for processing sweet corn valued at $325 per 0.4 ha and at about 1% Stewart's wilt incidence for fresh market sweet corn valued at $1,625 per 0.4 ha. Relatively small differences in levels of control conferred by commercially available rates of clothianidin (0.25 mg a.i. per kernel) and thiamethoxam (0.125 mg a.i. per kernel) were of little consequence in processing sweet corn but had considerable economic value in fresh market sweet corn.

Evaluation of Food-Grade Dent Corn Hybrids for Severity of Fusarium Ear Rot and Fumonisin Accumulation in Grain.

Fumonisins produced by Fusarium verticillioides (syn = F. moniliforme) and F. proliferatum have been associated with potentially serious toxicoses of animals and humans. Thus, hybrids with low fumonisin accumulation in grain will be valuable for the production of corn-based human food products. We evaluated 68 food-grade dent corn hybrids for severity of Fusarium ear rot and fumonisin accumulation in grain in inoculated trials in Urbana, IL in 2000 and 2001. Our inoculation technique was successful in initiating fumonisin accumulation that allowed discrimination among hybrids. We identified several hybrids that could have acceptable levels (<4 µg/g) of fumonisin accumulation in Illinois in most years. Twenty-six hybrids with low or high fumonisin accumulation in 2000 were reevaluated in noninoculated trials at three locations in Illinois in 2001. Fumonisin concentration in grain at all three locations was relatively low; thus, separation of hybrids was poor. At two locations, those hybrids with the highest fumonisin concentration in grain also had high concentrations following inoculation. However, one hybrid that had relatively low fumonisin concentration following inoculation had unacceptable levels of fumonisin (5 µg/g) in natural conditions. Therefore, hybrids need to be evaluated by inoculation and further evaluated at locations where the environment favors fumonisin accumulation.

Ability of an ELISA-Based Seed Health Test to Detect Erwinia stewartii in Maize Seed Treated with Fungicides and Insecticides.

Two sets of experiments were done to examine whether seed-treatment chemicals affected the ability of an enzyme-linked immunosorbent assay (ELISA)-based seed health test to detect Erwinia stewartii. The chemicals evaluated included Actellic, Apron, Captan, Cruiser, Gaucho, Maxim, Poncho, Thiram, and Vitavax in 11 seed-treatment combinations. In one experiment, seed-treatment chemicals were evaluated quantitatively in a critical region of ELISA absorbance values near 0.5 using maize seed that were spiked with uniform quantities of a liquid suspension of E. stewartii. The number of bacteria in each sample was estimated from ELISA absorbance values using standard curves. Log CFU of E. stewartii per sample were not significantly different among the untreated control and the 11 seed treatments compared with Tukey's Studentized Range Test (P = 0.05). Means of log CFU/ml for all treatments were tightly clustered around 5.70 which corresponded to an absorbance value of 0.440 and a bacterial population of about 500,000 CFU/ml. In a second set of experiments, seed treatment chemicals were evaluated based on qualitative decisions that resulted from the ELISA-based seed health test of seed lots of Jubilee and A632 infected with E. stewartii. The number of negative samples was not substantially greater than expected based on binomial probabilities except for samples of Captan/Vitavax-treated A632, which we considered to be a type I error. The mean absorbance values of positive samples ranged from 1.42 to 1.72 for A632 and from 1.51 to 1.91 for Jubilee and did not differ significantly among the seed treatments. There was no consistent evidence from these experiments that fungicide or insecticide seed treatments interfered with the sensitivity of the ELISA or altered low (e.g., 0.5) or high (e.g. 1.4 to 1.9) absorbance values. The ability of the ELISA-based seed health test to detect E. stewartii in maize seed was not affected by these seed treatments.

Sources of resistance to fumonisin accumulation in grain and fusarium ear and kernel rot of corn.

ABSTRACT Fumonisin is a group of homologous mycotoxins produced by several species of Fusarium. Fumonisin has been associated with Fusarium ear and kernel rot of corn (Zea mays) and several toxicoses of animals and humans. Corn inbreds with a high level of resistance to fumonisin production and accumulation in grain have not been identified. The objective of this study was to evaluate a genetically diverse collection of inbreds as potential sources of resistance to fumonisin production and accumulation in grain and Fusarium ear and kernel rot when crossed with a commercial "B73-type" line. F(1) hybrids developed with the inbred FR1064 and 1,589 and 1,030 inbreds were evaluated in inoculated and naturally infected trials, respectively, in 2000. Thirty-five F(1) hybrids with fumonisin concentration in grain of

Relationships Between Reactions of Sweet Corn Hybrids to Stewart's Wilt and Incidence of Systemic Infection by Erwinia stewartii.

Relationships between the reactions of sweet corn hybrids to Stewart's wilt and the incidence of natural, systemic infection by Erwinia stewartii differed among trials in which the prevalence of Stewart's wilt differed. Systemic Stewart's wilt infection was assessed for 262, 296, and 245 hybrids planted in seven trials in central Illinois in June and July 1998, 1999, and 2000, respectively. Incidence of systemic infection was calculated in each trial for all hybrids in each of nine categories of Stewart's wilt reactions (i.e., 1 = resistant and 9 = susceptible). When mean incidence was about 5%, incidence ranged from about 1 to 8% on resistant to moderately susceptible hybrids, but incidence was nearly 30% on susceptible hybrids. When mean incidence ranged from 10 to 16%, the relationships between hybrid reactions and incidence were explained by exponential or polynomial regressions. Incidence was less than 10% for hybrids with resistant and moderately resistant reactions, and incidence was greater than 15% for moderately susceptible to susceptible hybrids. When mean incidence was near 50%, the relationship was linear. Incidence was about 18% for resistant hybrids and about 80% for susceptible hybrids. Incidence increased about 8% for each class of hybrid reaction from 1 to 9. The influence of resistance on the development of systemic infection at very early seedling growth stages also was evaluated in six greenhouse trials. A highly resistant hybrid, Bonus, was systemically infected in two of six greenhouse trials when seedlings were inoculated prior to the V3 growth stage; however, systemic infection was not as severe as on a susceptible hybrid, Jubilee. Systemic infection was more severe on Bonus when plants were inoculated at earlier growth stages between VE and V3. The resistant hybrid Bonus was not systemically infected when inoculated after the V4 growth stage except for one greenhouse trial when all Stewart's wilt ratings were higher than usual. Hybrid reactions to Stewart's wilt affected the incidence of systemic infection in field situations and they affected the growth stage at which resistance effectively prevented systemic movement of E. stewartii within plants in greenhouse trials. This information can be used to determine more effectively when to apply other control measures, such as insecticidal seed treatments.

Evaluation of Inoculation Techniques for Fusarium Ear Rot and Fumonisin Contamination of Corn.

Fumonisins have been associated with potentially serious toxicoses of animals and humans. Prior to initiating a corn (Zea mays) breeding program for resistance to these mycotoxins, an efficient inoculation technique must be developed. Four inoculation techniques were evaluated on 14 commercial corn hybrids in Urbana, IL in 1999 and 2000. The techniques were: injection of inoculum through the ear husk leaves at R2 (blister); silks sprayed with inoculum at R2 and covered with a shoot bag until harvest; silks sprayed with inoculum at R2, covered with a shoot bag, reinoculated 1 week thereafter, and covered with a shoot bag until harvest; and insertion of six Fusarium-colonized toothpicks into the silk channel at R2. Only injection of inoculum through the husk leaves significantly increased the concentration of fumonisin in grain and severity of Fusarium ear rot compared with a control. This technique effectively differentiated hybrids previously identified as resistant or susceptible to Fusarium ear rot. The rank order of hybrids inoculated with this technique did not significantly change in the 2 years of this study. This technique is suitable for efficiently evaluating a large number of corn genotypes for resistance to Fusarium ear rot and fumonisin concentration.

Rates of Transmitting Erwinia stewartii from Seed to Seedlings of a Sweet Corn Hybrid Susceptible to Stewart's Wilt.

Rates of transmitting Erwinia stewartii from seed to seedlings were estimated from field grow-outs of seedlings grown from seed infected with E. stewartii. Infected seed were produced in 1998, 1999, and 2000 on a Stewart's wilt-susceptible sweet corn hybrid, Jubilee. Seedlings were inoculated repeatedly with pinprick inoculators and suspensions of E. stewartii were injected into ear shanks of the primary ears of each adult plant. Seed from inoculated plants were harvested and bulked. Single kernels were assayed for E. stewartii to estimate the proportion of kernels infected with E. stewartii. Estimates of E. stewartii-infection were 15.6 ± 4.3, 49.4 ± 3.9, and 12.5 ± 2.4% for seed produced in 1998, 1999, and 2000, respectively. Approximately 61,800 seedlings were grown in DeKalb, IL in 1999 and 83,400 and 60,000 seedlings were grown in Plover WI in 2000 and 2001, respectively, from infected seed lots produced the previous year. Approximately 10,000, 12,200, and 29,400 seedlings of susceptible sweet corn hybrids also were grown each year from commercial seed produced in Idaho where Stewart's wilt does not occur. Based on estimates of kernel infection in each seed lot and plant populations in each grow-out trial, about 9,600, 41,200, and 7,500 seedlings were grown from infected kernels in 1999, 2000, and 2001, respectively. Seedlings at the two- to three-leaf stage were examined for symptoms of Stewart's wilt. Infected plants were confirmed by microscopic observations of bacterial ooze and by enzyme-linked immunosorbent assay. When data were combined from all three trials, 59 of approximately 58,300 seedlings grown from infected seed were infected with E. stewartii based on symptoms of Stewart's wilt and E. stewartii-positive leaf tissue samples. Of these 59 seedlings, 22 probably were infected from seed-to-seedling transmission of E. stewartii and 37 probably were the result of natural infection due to the presence of flea beetles in DeKalb in 1999. Twenty-two infected seedlings from 58,300 infected kernels corresponds to a seed-to-seedling transmission rate of 0.038%. This rate of seed-to-seedling transmission of E. stewartii is substantially lower than seed transmission rates reported in the first half of the twentieth century; however, it is similar to seed-to-seedling transmission rates reported from other recent research.

Transmission of Erwinia stewartii from Plants to Kernels and Reactions of Corn Hybrids to Stewart's Wilt.

Stewart's wilt reactions of 98 food-grade, white corn hybrids, 3 yellow dent corn hybrids, and 23 sweet corn hybrids and infection of kernels by E. stewartii were evaluated in 1998, 1999, and 2000. Stewart's wilt symptoms were rated from 1 (no appreciable spread of symptoms) to 9 (dead plants) following inoculation. The mean Stewart's wilt ratings for the food-grade, white corn and yellow dent corn hybrids were 1.9, 2.4, and 2.9 in 1998, 1999, and 2000, respectively. The mean Stewart's wilt ratings for the sweet corn hybrids were 3.8, 4.2, and 4.6 in 1998, 1999, and 2000, respectively. Hybrids with ratings less than 3 were classified as resistant. Hybrids with ratings between 3 and 4.5 were classified as moderate. Hybrids with ratings greater than 4.5 were classified as susceptible. Ears harvested from each row in 1998 and 1999 were assayed for E. stewartii using an enzyme-linked immunosorbent assay (ELISA)-based seed health test. Kernels from 16 hybrids were positive for E. stewartii in 1998. Kernels from 11 hybrids were positive for E. stewartii in 1999. Kernel infection by E. stewartii was affected considerably by the level of host resistance (i.e., reactions of seed parent plants). For hybrids classified as resistant, estimates of kernel infection were 0.024 and 0.0007% in 1998 and 1999, respectively. For hybrids with moderate reactions to Stewart's wilt, estimates of kernel infection were 0.19 and 0.07% in 1998 and 1999, respectively. For hybrids with susceptible reactions to Stewart's wilt, estimates of kernel infection were 11.6 and 7.8% in 1998 and 1999, respectively. Based on high levels of Stewart's wilt resistance in food-grade, white corn hybrids, and low rates of kernel infection by E. stewartii in resistant and moderate hybrids, there is an exceedingly low probability of introducing E. stewartii to areas where it does not occur by transmitting the bacterium in grain of the food-grade, white corn hybrids evaluated in this study. Although all of the kernels harvested in these experiments were produced as grain on open-pollinated F1 hybrids, the rates of kernel infection observed for hybrids with resistant, moderate and susceptible reactions to Stewart's wilt are applicable to seed produced on inbred lines with equivalent Stewart's wilt reactions.

Quantitative Trait Loci in Sweet Corn Associated with Partial Resistance to Stewart's Wilt, Northern Corn Leaf Blight, and Common Rust.

ABSTRACT Partial resistance to Stewart's wilt (Erwina stewartii, syn. Pantoea stewartii), northern corn leaf blight (NCLB) (Exserohilum turcicum), and common rust (Puccinia sorghi) was observed in an F(2:3) population developed from a cross between the inbred sweet corn lines IL731a and W6786. The objective of this study was to identify quantitative trait loci (QTL) associated with partial resistance using restriction fragment length polymorphic markers. Phenotypic data were collected for 2 years for Stewart's wilt, NCLB, and common rust but, due to significant family-environment interaction, analysis was conducted individually on data from each year. In 2 years of evaluation for the three diseases, a total of 33 regions in the maize genome were associated with partial resistance describing from 5.9 to 18% of the total phenotypic variability. Of six regions common in both years, three were associated with partial resistance to Stewart's wilt (chromosomes 4:07, 5:03, and 6:04), one was associated with NCLB (chromosome 9:05), and two were associated with common rust (chromosomes 2:04 and 3:04). The rust QTL on 3S mapped to within 20 cM of the rp3 locus and explained 17.7% of the phenotypic variability. Some of the QTL associated with partial resistance to the three diseases have been reported previously, and some are described here for the first time. Results suggest it may be possible to consolidate QTL from various elite backgrounds in a manner analogous to the pyramiding of major resistance genes. We also report here on two QTL associated with anthocyanin production on chromosomes 10:6 and 5:03 in the general location of the a2 gene.

Puccinia sorghi Virulent on Sweet Corn with the Rp1-D Gene in Southern France.

The Rp1-D gene, which conveys a chlorotic-fleck resistant reaction to Puccinia sorghi, effectively controlled common rust on sweet corn in North America for nearly 15 years. Biotypes of P. sorghi virulent on plants with the Rp1-D gene were widespread in North America for the first time in 1999 and again in 2000 (1,2). Many Rp-resistant sweet corn hybrids that are developed and grown in North America also are grown in Europe, including France where virulence against the Rp1-D gene has not been reported previously. In September 2000, uredinia of common rust were observed on and collected from sweet corn hybrids with the Rp1-D gene in commercial fields and hybrid trials in the Landes and Pyrénées Atlantiques departments of the Aquitaine region of southwestern France. Severity of rust generally was below 5% on these plants except for a few hybrids for which severity was about 20 to 30%. Common rust was not observed on hybrids with the Rp-G gene. Urediniospores were increased as a bulk population on the susceptible sweet corn hybrid Sterling in a greenhouse. Plants with each of 10 single Rp genes (Rp1-A, Rp1-C, Rp1-D, Rp1-E, Rp1-F, Rp1-I, Rp1-K, Rp1-L, Rp1-N, and Rp-G) or each of six compound rust resistance genes (Rp1-D5, Rp1-JC, Rp1-JFC, Rp-GDJ, Rp-GFJ, and Rp-G5JC) were assayed for reactions to this population of P. sorghi. Two to six different sources of seed of each single Rp gene and two different sources of seed of each compound rust resistance gene were replicates with a single pot of 6 to 18 plants grown from a specific seed source. Plants were inoculated three times on successive days by placing 2 or 3 ml of a urediniospore suspension in the whorl of two- to four-leaved seedlings. Reactions were rated 10 days after the last inoculation. Plants without symptoms or with chlorotic-fleck resistant reactions were inoculated again and rated 10 days later. Uredinia did not form on plants with compound rust resistance genes. Plants with the genes Rp1-E, Rp1-I, Rp1-K, and Rp-G also were resistant although a few, very small uredinia (i.e., type-1 uredinia) were observed on a few plants. Plants with the genes Rp1-A, Rp1-C, Rp1-D, Rp1-F, Rp1-L, and Rp1-N were fully susceptible. This pattern of virulence is the same as that observed during the past two years in North American populations of P. sorghi virulent against Rp1-D. Rp-resistance currently available in most sweet corn hybrids will not be effective in France if these virulent biotypes become prevalent. References: (1) J. K. Pataky et al. Plant Dis. 85:165, 2001. (2) M. C. Pate et al. Plant Dis. 84:1154, 2000.

Control of Stewart's Wilt in Sweet Corn with Seed Treatment Insecticides.

Corn flea beetles, Chaetocnema pulicaria, vector Erwinia stewartii (synamorph Pantoea stewartii), which causes Stewart's bacterial wilt of corn (Zea mays). A seed treatment insecticide, imidacloprid, killed flea beetles and reduced the number of feeding wounds and Stewart's wilt symptoms per leaf in greenhouse studies. The objective of our research was to evaluate the ability of imidacloprid and thiamethoxam seed treatments to control Stewart's wilt on sweet corn hybrids under field conditions with naturally occurring populations of the corn flea beetle. Six field trials were planted at four locations in 1998. Eleven field trials were planted at nine locations in 1999. The treatment design was a factorial of sweet corn hybrids and seed treatments. Stewart's wilt incidence ranged from 0 to 54% in the 1998 trials. Incidence of Stewart's wilt in nontreated plots of the susceptible hybrid Jubilee ranged from 2% at the 8-leaf stage to 77% 1 week after mid-silk in the 1999 trials. Seed treatment insecticides reduced the incidence of Stewart's wilt by ≈50 to 85% relative to nontreated controls. The level of control was ≈75 to 85% in seven trials planted before 1 June 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 4 to 71%. The level of control was ≈50 to 70% in the three trials planted after 1 July 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 44 to 73%. Although comparisons varied, the level of control gained from seed treatment insecticides was similar to the next higher level of host resistance. Seed treatment insecticides appear to control Stewart's wilt during very early growth of corn plants, when foliar applications of insecticides are ineffective and the effectiveness of host resistance varies depending on the proximity of flea beetle feeding sites to the plant's growing point.

First Report of Puccinia sorghi Virulent on Sweet Corn with the Rp1-D Gene in Florida and Texas.

For the past 15 years, the Rp1-D gene has controlled common rust on sweet corn in North America. In August and September 1999, isolates of Puccinia sorghi were collected from Rp1-D sweet corn hybrids in Illinois, Wisconsin, Minnesota, Michigan, and New York. This was the first widespread occurrence in the continental United States of P. sorghi virulent on the Rp1-D gene (1). Isolates of P. sorghi collected from Los Mochis, Mexico, in March 2000 had a pattern of virulence similar to the pattern for the isolates collected in the Midwest in 1999 (2). In April and May 2000, small uredinia were observed on Rp1-D sweet corn in Florida and Texas. In Florida, isolates were collected from six different locations within a 13-km radius near Belle Glade. Three isolates were collected each from Rp1-D and non-Rp sweet corn hybrids. Isolates also were collected from two Rp1-D sweet corn hybrids and a non-Rp sweet corn hybrid near Hondo, TX. Inocula of isolates were increased through one uredinial generation in the greenhouse. Several 1-cm2 pieces of leaf tissue with sporulating uredinia were placed in 15 ml of a solution of water and Tween 20. This inoculum was placed in whorls of five two-leaved seedlings of a susceptible hybrid, 'Primetime.' Urediniospores from newly formed uredinia were collected 10 days later and used as inocula to assay each isolate. Two isolates from Florida (one each from an Rp1-D and a non-Rp hybrid) were assayed on a non-Rp susceptible check, 20 different single Rp genes, and nine compound Rp genes. Other isolates were assayed on two replicates of a non-Rp susceptible check, a source of Rp1-D, and five single Rp genes that were effective against the isolates collected from the Midwest in 1999 and from Mexico in 2000. Each experimental unit consisted of five plants grown in 10-cm-diameter pots. Plants at the two-leaf stage were inoculated three times within 5 days by filling whorls with a urediniospore suspension. Rust reactions were rated 10 days after the final inoculation. Isolates collected in Florida from non-Rp hybrids were avirulent on Rp1-D but those collected in Texas from non-Rp hybrids were virulent on Rp1-D. Isolates collected in Florida and Texas from Rp1-D hybrids had a similar pattern of virulence as isolates collected from the Midwest in 1999 and from Mexico in March 2000; that is, effective single Rp genes included Rp1-E, Rp-G, Rp1-I, and Rp1-K. A source that we previously believed was Rp1-L now appears to be Rp-G. These are the first reports from Florida and Texas of P. sorghi virulent on Rp1-D, and they are the first occurrences of virulence against Rp1-D in the continental U.S. in 2000. Apparently, P. sorghi with virulence against Rp1-D has become established in an area where common rust inocula for North America overwinters. References: (1) J. K. Pataky and W. F. Tracy. Plant Dis. 83:1177, 1999. (2) J. K. Pataky et al. Plant Dis. 84:810, 2000.