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Genetics

Accumulation of Minor Gene Resistance to Peronospora trifoliorum in Diploid Alfalfa. D. Z. Skinner, Research assistant, Department of Plant Pathology, Throckmorton Hall, Kansas State University, Manhattan 66506, Present address: Department of Plant Pathology, University of Wisconsin, Madison 53706; D. L. Stuteville, Professor, Department of Plant Pathology, Throckmorton Hall, Kansas State University, Manhattan 66506. Phytopathology 79:721-724. Accepted for publication 17 January 1989. Copyright 1989 The American Phytopathological Society. DOI: 10.1094/Phyto-79-721.

The inheritance of diploid Medicago sativa resistance to Peronospora trifoliorum, because of genes with small, cumulative effects, was studied. Infection types (ITs) were described on a 0 (no conidial production) to 5 (copious conidial production) scale. Plants P1 and P2, whose S₁ populations were 0 and 3% resistant (IT = 0) to isolate I-7, were crossed and their F₁ populations were selected for resistance to I-7. Progeny of the selected plants had increased resistance not only to I-7, but also to pathogenically different isolates I-5 and I-8, which suggested that the increased resistance was general in nature. Two F₁ plants of P1 and P2, whose S₁ populations were 59 and 37% resistant to I-7, were crossed. Two of their progeny, whose S₁ populations were 73 and 76% resistant to I-7, also were crossed. Both resistant and susceptible progeny of this cross were selfed. Segregation in S₁ populations of the resistant plants indicated that the apparent general resistance was due to a collection of isolate-specific interactions. Plants with 98% of their S₁ progeny resistant to I-7 were derived from P1 × P2 crosses. However, virtually none of this resistance was expressed in the progeny of a backcross to P1. These results indicated that high levels of minor gene resistance were derived from plants with no readily apparent resistance without fixing the genes for resistance, and that minor gene resistance generally was not expressed in progeny of a resistant-by-susceptible cross. Hence, the expression of minor gene resistance was dependent on genetic background and may have been masked by epistatic susceptibility.