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The effects of bed height, mulches, composted poultry litter, and cultivars on Phytophthora crown rot, caused by Phytophthora capsici Leonian, of summer squash (Cucurbita pepo L.) were evaluated in the absence of fungicide applications. The experimental design was a split-split-split plot arrangement of a randomized complete block. Bed height (flat or raised) was the main plot treatment. Mulches (bare soil, wheat straw, or plastic) were subplot treatments. Composted poultry litter applications (0 or 4.5 t·ha⁻¹) were sub-subplot treatments. Squash cultivars (Cougar or Payroll) were sub-sub-subplot treatments. Incidence of plant death (%) was assessed from 0 to 35 days post-inoculation (dpi) with P. capsici. Plant death 35 dpi and area under the disease progress curve (AUDPC)differed significantly (P < 0.0001) between the cultivars Cougar and Payroll. Mean plant death 35 dpi was 87% for ‘Payroll’ and 99% for ‘Cougar’. The bed height × cultivar interaction was also significant (P = 0.0018) in the analyses of variance for plant death and AUDPC. Plant death at 35 dpi and AUDPC for ‘Payroll’ were greater in flat beds than raised beds. Disease was unaffected by the main effects of bed height, mulch type, or application of poultry litter. Thirty-two summer squash cultivars and 10 germplasm accessions were also evaluated for resistance to Phytophthora crown rot in a separate greenhouse trial. Crown rot severity was rated on a 1 (no symptoms) to 5 (plant death) scale at 18 dpi. Crown rot severity differed significantly (P < 0.0001) among cultivars and germplasm accessions. Crown rot severity averaged 4.3 on commercial cultivars and 2.2 on germplasm accessions. Crown rot was least severe on the commercial cultivar Spineless Beauty (mean rating = 2.9). No disease developed on four accessions of Cucurbita moschata previously reported to be crown rot-resistant.

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.

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.

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.