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First Report of a Wheat Leaf Rust (Puccinia triticina) Phenotype with High Virulence to Durum Wheat in the Great Plains Region of the United States
- Kolmer, J. A.
- Plant disease 2015 v.99 no.1 pp. 156
- Puccinia recondita, Triticum turgidum, alleles, chlorosis, color, cultivars, durum wheat, genotype, genotyping, hard red spring wheat, hard red winter wheat, hexaploidy, leaf rust, leaves, mature plants, microsatellite repeats, necrosis, pedigree, phenotype, plant pathogenic fungi, seedlings, surveys, tetraploidy, urediniospores, virulence, Arizona, California, Great Plains region, Kansas, Mediterranean region, Mexico, Middle East, North Dakota, Saskatchewan
- Phenotypes of the wheat leaf rust pathogen Puccinia triticina with high virulence to tetraploid durum wheat (Triticum turgidum) are found regularly in Mexico (5), the Mediterranean region (1), the Middle East (3), and rarely in the Imperial Valley of California and the adjacent area in Arizona. Previous to 2013, these phenotypes had not been found in the Great Plains region of the United States where hexaploid, T. aestivum types of hard red winter wheat, hard red spring wheat, and durum wheat are grown. In May 2013, collections of P. triticina, the wheat leaf rust fungus identified by color, size, and shape of uredinia, were obtained from leaves of the hard red winter wheat cultivar Overley in research plots at Hutchinson, KS. A single uredinial isolate was obtained that was used in virulence testing and molecular genotyping. Urediniospores from the initial field collection were inoculated onto seedlings of the susceptible cultivar Little Club. Subsequently, single uredinia were isolated and re-increased on Little Club. The single uredinial isolate was initially inoculated to 7-day-old seedlings of 20 lines of Thatcher wheat that are near-isogenic for leaf rust resistance genes and are used in the annual virulence surveys of P. triticina in the United States (2). The phenotype of the isolate, based on virulence to the 20 differential lines, was BBBQD (2), which was identical to phenotypes of P. triticina with high virulence to durum wheat from other regions where durum wheat is commonly grown (4). This phenotype had intermediate infection type of 2⁺ (moderate size uredinia with chlorosis) to the line with Lr2c and high infection types of 3⁺ (large uredinia with no chlorosis or necrosis) to lines with genes LrB, Lr10, and Lr39/41. Overley wheat has Lr39/41. The isolate was further tested on an additional set of 27 Thatcher lines, the cultivar Gatcher with Lr27 + Lr31, and a set of 15 durum wheat cultivars that have been grown in the United States and Canada. The isolate had virulence to lines with genes Lr14b, Lr20, Lr23, Lr33, Lr44, and Lr64. Notably, the isolate had distinct low infection types to seedlings of Thatcher lines with genes Lr12, Lr13, Lr22a, Lr35, and Lr37 that are usually optimally expressed in adult plants to most P. triticina isolates. The isolate had high virulence to all of the durum wheat cultivars. The single uredinial isolate of P. triticina from Overley was also genotyped with microsatellite alleles used in previous studies with P. triticina collections from durum wheat (3). The isolate from Kansas had a highly similar genotype to other isolates of P. triticina from worldwide durum-producing regions (3). This isolate with high virulence to durum wheat most likely migrated to the southern Great Plains region from the durum-growing regions in Mexico. Cultivars such as TAM 112, Armour, Winterhawk, and Bullet with Lr39/41 and other cultivars with Overley in their pedigree are currently grown throughout the southern Great Plains. Since many of the P. triticina phenotypes with high virulence to durum wheat are virulent to Lr39/41, these cultivars may provide a pathway for the spread of these phenotypes to the major durum-producing areas of North Dakota and Saskatchewan.References: (1) H. J. Goyeau et al. Plant Pathol. 61:761, 2012. (2) J. A. Kolmer and M. A. Hughes. Plant Dis. 97:1103, 2013. (3) M. E. Ordoñez and J. A. Kolmer. Phytopathology 97:574, 2007. (4) M. E. Ordoñez and J. A. Kolmer. Phytopathology 97:344, 2007. (5) R. P. Singh et al. Plant Dis. 88:703, 2004.