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.
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.