VIEW ARTICLE

Resistance

Characteristic Cellular Responses as Expression of Genes for Resistance to Erysiphe graminis f. sp. hordei in Barley. Hironori Koga, Laboratory of Plant Pathology, Faculty of Agriculture, Kyoto University, Kyoto 606, Japan, Present address: Hokuriku National Agricultural Experiment Station, Joetsu-shi, Niigata 943-01, Japan; Hideyoshi Toyoda(2), Shigeyuki Mayama(3), Jiko Shishiyama(4), and Unji Hiura(5). (2)Laboratory of Plant Pathology, Faculty of Agriculture, Kyoto University, Kyoto 606, Japan, Present address: Laboratory of Plant Pathology, Faculty of Agriculture, Kinki University, Higashi-Osaka 577, Japan; (3)Laboratory of Plant Pathology, Faculty of Agriculture, Kyoto University, Kyoto 606, Japan, Present address: Laboratory of Plant Pathology, Faculty of Agriculture, Kagawa University, Miki-cho 761-07, Japan; (4)Laboratory of Plant Pathology, Faculty of Agriculture, Kyoto University, Kyoto 606, Japan; (5)Institute of Agricultural and Biological Science, Okayama University, Kurahsiki 710, Japan. Phytopathology 73:907-910. Accepted for publication 7 January 1983. Copyright 1983 The American Phytopathological Society. DOI: 10.1094/Phyto-73-907.

The relationship between fungal development and host cellular responses in barley plants inoculated with Erysiphe graminis f. sp. hordei was evaluated in cultivars with different single alleles and multiple alleles for resistance at the JM1_sn locus and in cultivars possessing two genes for resistance. With increased levels of resistance fewer infection attempts continued beyond the penetration stage. Cessation of fungal growth was most strongly associated with penetration attempts that ended in formation of a papilla and an intensely fluorescent cytoplasmic aggregation. In the multiple allelic lines of JM1_sn locus, the cessation of fungal growth followed by the appearance of fluorescence of epidermal cells was highly correlated with the degree of resistance. The results suggested that the genes for resistance could determine a recognition event, controlling the rate of degree of cytoplasmic aggregation followed by the formation of fluorescent collapsed cells in the incompatible interactions.