VIEW ARTICLE

Resistance

Race Composition and Pathogenicity Associations of Rhynchosporium secalis in California. Qifa Zhang, Biotechnology Center, Huazhong Agricultural University, Wuhan, China; R. K. Webster(2), B. A. Crandall(3), L. F. Jackson(4), and M. A. Saghai Maroof(5). (2)Department of Plant Pathology, University of California, Davis 95616; (3)BHN Research, Western Division, Watsonville, CA 95076; (4)Department of Agronomy and Range Science, University of California, Davis 95616; and (5)Department of Crop and Soil Environmental Sciences, Virginia Polytechnic Institute and State University, Blacksburg 24061. Phytopathology 82:798-803. Accepted for publication 17 April 1992. Copyright 1992 The American Phytopathological Society. DOI: 10.1094/Phyto-82-798.

Data from a pathogenicity study involving 723 isolates of Rhynchosporium secalis, the causal agent of barley scald, were analyzed for race composition and pathogenicity associations. Isolates were collected from California in 1973, 1983, and 1984. The results showed that the collection made in 1973 differed drastically in race composition from the collections of 1983 and 1984. The 1973 collection was composed mostly of simple races that were capable of producing disease on a few host differentials. The two later collections contained large proportions of complex races that were pathogenic on a large number of differentials. The majority of the pairwise correlations between pathogenicity on different host differentials were highly significant in all three collections, which indicated close associations of genes for pathogenicity among isolates of this fungus. In contrast to the large difference in race composition, most of the significant correlations were in the same direction (positive or negative) in all three collections. The overall structure of pathogenicity association, as determined by cluster analysis, also was very similar for isolates in all three collections. It is inferred that the highly conserved pathogenicity associations were at least partly due to natural selection favoring the development and maintenance of particular pathogenic gene combinations in the fungal populations.