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Resistance

Chlorotic Lesion Response of Maize to Cercospora zeae-maydis and Its Effect on Gray Leaf Spot Disease. J. T. Freppon, Former research associate, associate professor, Department of Horticulture and Crop Science, and professor, Department of Plant Pathology, The Ohio State University, Ohio Agricultural Research and Development Center, Wooster 44691, respectively; R. C. Pratt, and P. E. Lipps. Former research associate, associate professor, Department of Horticulture and Crop Science, and professor, Department of Plant Pathology, The Ohio State University, Ohio Agricultural Research and Development Center, Wooster 44691, respectively. Phytopathology 86:733-738. Accepted for publication 29 March 1996. Copyright 1996 The American Phytopathological Society. DOI: 10.1094/Phyto-86-733.

Chlorotic lesions (CL) developed on certain F_2:3 and F_3:4 families derived from a cross between a previously described CL-resistant maize inbred (NC250A) and a susceptible (S) lesion maize inbred (B73) in response to infection by Cercospora zeae-maydis. CL trait expression was consistent (displayed phenotype across locations at midepidemic assessment) on 12 of the 60 F_2:3 families studied. Heterogeneous (CL/S) lesion phenotypes were displayed by 36 families at midepidemic. Consistent, characteristic S lesions were exhibited by 12 F_2:3 families. Selected F_2:3 families representing each lesion type class produced F_3:4 progenies that predominantly displayed lesion phenotypes consistent with the parental class. Families exhibiting the CL trait at midepidemic assessment had significantly lower apparent infection rates, percent leaf area affected (PLAA), and area under disease progress curves based on PLAA and lesion area. Heterogeneous families tended to have intermediate mean gray leaf spot severity, whereas disease severity and progress were highest on homozygous S lesion-type families. Because the CL trait was associated with decreased gray leaf spot severity and progress, selection for this trait in a population derived from NC250A × B73 would decrease the impact of epidemics caused by C. zeae-maydis. Segregation analyses of midepidemic CL responses of F_2:3 and F_3:4 families during 1992 and 1993 suggested the presence of a major factor in inheritance of the CL response. Segregation ratios observed at a later assessment date during 1992 did not support monogenic inheritance.