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Pathogenicity Associations in Puccinia graminis f. sp. tritici in the United States. Helen Miller Alexander, Former research associate, Department of Plant Pathology, University of Minnesota, St. Paul 55108, Present address: Department of Biology, University of Louisville, Louisville, KY 40292; A. P. Roelfs(2), and J. V. Groth(3). (2)Research plant pathologist, Cereal Rust Laboratory, ARS, USDA, St. Paul, MN 55108; (3)Associate professor, Department of Plant Pathology, University of Minnesota, St. Paul 55108. Phytopathology 74:1161-1166. Accepted for publication 20 March 1984. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1984. DOI: 10.1094/Phyto-74-1161.

Associations of pathogenicity in predominantly asexually reproducing populations of Puccinia graminis f. sp. tritici were analyzed for eight selected years between 1929 and 1978 on 10 standard differential wheat lines. In 1975, pathogenicity associations on 16 “single gene” lines were examined for sexual and asexual fungal populations. Associations were frequent and highly significant in all years of testing with the standard differential lines; for one-fourth of the paired combinations, the association vacillated from positive to negative over the eight years. Associations of pathogenicity were much more frequent and stronger in the asexual than in the sexual population in 1975. These data provide evidence that, in asexually reproducing populations of P. graminis f. sp. tritici, virulences and avirulences are effectively linked; thus, selectively important associations and associations occurring by chance are indistinguishable. Associations found in sexual populations are more likely to be maintained by selection. Negative associations for pathogenicity existed for host gene pairs Sr7b/15, 11/9a, 8/15, 8/17, 9a/10, 9a/Tmp, 9a/9e, and 36/15 in the sexual population. Experiments are advocated to find if selection for increased pathogen fitness on one host genotype leads to decreased fitness on other host genotypes. Combinations of resistance genes for which pathogens have low fitness could be introduced into cultivars for potentially more durable rust resistance.