Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/7/2005
Publication Date: 7/10/2005
Citation: Faris, J.D., Friesen, T.L. 2005. Identification of quantitative trait loci for race-nonspecific resistance to tan spot in wheat. Theoretical and Applied Genetics. Vol. 111:386-392. Interpretive Summary: Tan spot is a foliar disease of wheat caused by a fungal pathogen (Pyrenophora tritici-repentis). Previously, genes for resistance to specific races of the tan spot pathogen have been identified. In this work, we evaluated resistance to races 1, 2, 3, and 5 in a population of wheat recombinant inbred lines. Our results indicate that, in this population, resistance to all four races is governed by common genes on the short arm of chromosome 1B and on the long arm of chromosome 3B. This is the first report of the identification of genes for race-nonspecific resistance to tan spot. Incorporation of these resistance genes into adapted wheat germplasm and cultivars will provide broad-spectrum resistance to at least four races of the tan spot pathogen.
Technical Abstract: Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is an economically important foliar disease in the major wheat growing areas throughout the world. Multiple races of the pathogen have been characterized based on their ability to cause necrosis and/or chlorosis on differential wheat lines. In this research, we evaluated a population of recombinant inbred lines derived from a cross between the common wheat varieties Grandin and BR34 for reaction to tan spot caused by Ptr races 1, 2, 3, and 5. Composite interval mapping revealed QTLs on the short arm of chromosome 1B and the long arm of chromosome 3B significantly associated with resistance to all four races. The effects of the two QTLs varied for the different races with the 1B QTL explaining from 13 to 29 percent of the phenotypic variation while the 3B QTL explained from 13 to 41 percent of the variation. Additional minor QTLs were detected, but not associated with resistance to all races. The host-selective toxin Ptr ToxA, which is produced by races 1 and 2, was not a significant factor in the development of disease in this population. The race-nonspecific resistance mechanisms derived from BR34 may preclude the recognition of the gene-for-gene interaction known to be associated with the wheat-tan spot system.