Molecular Mapping of a Stripe Rust Resistance Gene in Spring Wheat Cultivar Zak

Abstract

Stripe rust (yellow rust), caused by Puccinia striiformis f. sp. tritici, is one of the most devastating foliar diseases of wheat (Triticum aestivum) worldwide. Growing resistant cultivars is the best approach for control of the disease. Although the stripe rust resistance in spring wheat cv. Zak has been circumvented by a group of races of the pathogen predominant in the United States since 2000, the resistance genes in Zak were unknown. To identify and map the genes for resistance to stripe rust, Zak was crossed with susceptible wheat genotype ‘Avocet Susceptible’. Seedlings of the parents and F1, F2, and F3 progeny were tested with P. striiformis f. sp. tritici races PST-43 and PST-45 under controlled greenhouse conditions. Genetic analysis determined that Zak has a single dominant gene, designated as YrZak, conferring race-specific all-stage resistance. Resistance gene analog polymorphism (RGAP), simple sequence repeat (SSR), and sequence-tagged site (STS) techniques were used to identify molecular markers linked to YrZak. A linkage group of three RGAP, three SSR, and three STS markers was constructed for YrZak using 205 F3 lines. Amplification of the complete set of Chinese Spring nulli-tetrasomic lines with RGAP marker Xwgp102 indicated that YrZak is present on chromosome 2B. The three SSR markers further mapped YrZak to the long arm of chromosome 2B. Amplification of chromosome 2B deletion lines with SSR marker Xgwm501 further confirmed that YrZak is on chromosome 2BL. To determine the genetic distance between YrZak and Yr5, which also is present on chromosome 2BL, 300 F2 plants from cross Zak/Yr5 were tested with PST-43. Six susceptible plants were identified from the F2 population, indicating that YrZak and Yr5 are ≈42 centimorgans apart. The results of race reactions and chromosomal locations indicated that YrZak is different from previously identified genes for resistance to stripe rust. This gene should be useful in monitoring virulence changes in the pathogen population and in studying host–pathogen interactions.