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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., Competing Interests: The author(s) declare no conflict of interest.

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.

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.

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 79field 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 seedtreatment 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 I 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 I % 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. [ABSTRACT FROM AUTHOR]

Gibberella ear rot, caused by Gibberella zeae, has increased in prevalence recently on late-season 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. [ABSTRACT FROM AUTHOR]

The Ht1 gene conveys a chiorotic-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. [ABSTRACT FROM AUTHOR]