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Resistance

Variability and Interaction Between Alfalfa Cultivars and Isolates of Phytophthora megasperma. M. A. Faris, Research scientist, Agriculture Canada, Ottawa Research Station, Ottawa, Ontario, Canada K1A 0C6; Phytopathology 75:390-394. Accepted for publication 27 September 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, 1985. DOI: 10.1094/Phyto-75-390.

Six isolates of Phytophthora megasperma f. sp. medicaginis (Pmm) were tested individually for levels of virulence on 15 alfalfa cultivars having varying degrees of resistance to Phytophthora root rot (PRR). Stability parameters for the disease severity index were calculated by following Eberhart and Russell's regression technique. These included: regression coefficient (b), deviation from regression (S²_d), and the coefficient of determination (r²). Cultivar x isolate interaction was caused by differences between the cultivars fitted regression lines and by differences in the R₁ and R₂ response parameters. Only three cultivars possessed stable resistance to PRR. Some others had a high level of resistance to the mildly virulent isolates, but they were severely infected by the highly virulent isolates. Two cultivars were susceptible to all isolates. Regardless of their virulence, all isolates had approximately equal response parameters; they inflicted the greatest damage on cultivars with the least resistance. However, it was clear that there were two levels of virulence among the isolates. The importance of interactions affecting infection by Pmm is illustrated in this work and the application of the genotype x environment interaction analysis to their study is demonstrated. A low disease severity index (performance) and sensitivity to different levels of virulence (stability) must be considered when selecting the best alfalfa genotypes. Therefore, a sample of Pmm chosen from within the area of adaptation should be used to screen alfalfa genotypes for resistance to PRR.