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Genetic Analysis of Barley Stripe Mosaic Virus. M. C. Edwards, Research plant pathologist, USDA/ARS, Department of Plant Pathology, North Dakota State University, Fargo 58105; R. G. Timian, research plant pathologist, USDA/ARS, Department of Plant Pathology, North Dakota State University, Fargo 58105. Phytopathology 76:360-365. Accepted for publication 7 November 1985. 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, 1986. DOI: 10.1094/Phyto-76-360.

Four barley stripe mosaic virus strains were used in pseudorecombination experiments to elucidate the roles of the individual RNA species in pathogenicity and symptomatology. Experiments with strains CV40 and CV52 indicated that RNA 1 controls pathogenicity to Rodney oats and Modjo-1 barley. Experiments with strains CV35 and CV42 supported this and further indicated that RNA 1 controls pathogenicity to Moreval and Silver King barleys. Pathogenicity to Chenopodium amaranticolor was determined by CV35 RNA 1, although isolates possessing CV42 RNA 1 and CV35 RNAs 2 and 3 were also pathogenic to C. amaranticolor. Symptom development required a more complex interaction of viral RNAs with the host. Pseudorecombinant isolates most virulent to barley in the CV52 x CV40 experiments were those with CV52 RNA 1 and CV52 RNA 2 or 3. Similarly, pseudorecombinant isolates with CV35 RNA 1 or 2 combined with CV35 RNA 3 induced more severe symptoms in barley than other RNA combinations. Homologous RNAs may be more compatible than heterologous RNAs, significantly affecting symptomatology. Symptoms on oats were more severe when RNA 3 was derived from the more virulent parental strain and milder when RNA 3 was derived from the less virulent parental strain.

Additional keywords: Avena sativa, Hordeum vulgare, reassortant.