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Yellow- and White-Endosperm Effects on Stewart’s Wilt of Maize. M. S. Kang, Associate professor, Department of Agronomy, Louisiana Agricultural Experiment Station, Louisiana State University Agricultural Center, Baton Rouge 70803-2110; M. S. Zuber, Professor emeritus, Department of Agronomy, University of Missouri, Columbia 65211. Phytopathology 78:909-911. Accepted for publication 25 January 1988. Copyright 1988 The American Phytopathological Society. DOI: 10.1094/Phyto-78-909.

Stewart’s wilt of maize (Zea mays), caused by Erwinia stewartii, has sporadically been an economically important disease in the central corn belt states in the United States. The major objectives of this investigation were to study via a diallel mating design the genetics of resistance to Stewart’s wilt in yellow- and white-endosperm maize. Natural Stewart’s wilt infection of a diallel cross involving yellow × yellow endosperm (20 single crosses including reciprocals) and white × white endosperm (20 single crosses including reciprocals) indicated that general combining ability effects were more important than specific combining ability effects. The mean Stewart’s wilt rating (visual scale: 1 = resistant, 5 = intermediate, and 10 = susceptible) was lower (P = 0.01) for white-endosperm single crosses (3.3) than that for yellow-endosperm single crosses (3.8). Heritability estimates from white-endosperm single crosses, yellow-endosperm single crosses, and across both endosperms were 70, 37, and 40%, respectively. We concluded that the white-endosperm gene (y) might be associated with some modifier genes that were responsible for greater genetic differentiation of the white-endosperm single crosses. Low heritability estimates for Stewart’s wilt suggested that progress from selection in the material studied would be slow.

Additional keywords: bacterial wilt, host-pathogen interaction.