Stem rust caused by Puccinia graminis f. sp. tritici (Pgt) is an important disease of wheat in the world. Pgt pathogen is constantly evolving and creating more virulent races that break down stem rust (Sr) resistance genes. As a result, many of Sr genes have become ineffective against new Pgt races. Exploring new sources of resistance to detect new Sr genes/QTLs is very important in order to introducing them into wheat breeding programs and developing resistant wheat cultivars. The objective of the present study was to evaluate 297 Iranian wheat genotypes for resistance to stem rust at seedling stage and to detect Sr resistance genes/QTLs through association mapping (AM).
A set of 297 Iran bread wheat cultivars and landraces were evaluated for infection type and latent period in four race of Pgt. Genotypic data of 282 genotypes were available, so AM was performed based on 282 genotypes. The results of population structure analysis showed that 277 genotypes clearly were distinguished in the three subpopulations and the other five genotypes were classified in the mixed group. The mean linkage disequilibrium decreased with increasing genetic distance. The markers did not have a uniform distribution on the genomes, so the share of each of the A, B and D genomes in commercial cultivars and landraces was approximately 37, 46 and 17%, respectively. Collectively, 69 QTLs for infection type and 62 QTLs for latent period of studied Pgt races were identified in the original dataset (P ≤ 0.001). In the imputed SNPs dataset, the number of QTLs for infection type increased to 504 QTL and for latent period increased to 454 QTLs (P ≤ 0.001).
Based on the results of this study, it can be concluded that the Iranian wheat genotypes are valuable source resistance to stem rust. By incorporating these genotypes into wheat breeding programs and optimizing effective resistance genes, an important step can be taken to prevent the threat of and the disease to ensure food security. This study provides additional useful information for selection of resistant genotypes against the disease by improving marker-assisted selection efficiency.