| Pyrenophora tritici-repentis (PTR) is considered one of the most devastating pathogens of wheat worldwide, although little is known about pathogenic and molecular diversity. In this study, over 400 isolates of PTR from Asia, Australia, Europe, North America and South America were tested for their virulence on differential wheat genotypes and analyzed for genetic variations at 12 simple-sequence repeat (SSR) loci. A subset of 50 PTR isolates from different countries were randomly selected and analyzed with AFLP primers, and compared with internal transcribed spacers (ITS4 & ITS5) and glyceraldehyde-3-phosphate dehydrogenase (gpd) sequences. Phenotypic data showed that PTR races 1, 2 and 5 were common across five populations. High levels of gene diversity (HS = 0.31 to 0.56) and significant (P < 0.05) gametic disequilibrium were observed. Further, corrected standardized fixation index (G" ST) value ranged from 0.042 to 0.265 among five populations. These results suggest that PTR populations have moderate to high levels of population differentiation, which undergo regular sexual recombination, and that these geographically separated populations are genetically differentiated.;A subset of 825 spring and winter wheat accessions were evaluated for seedling resistance to PTR race 1, and 215 wheat accessions exhibited resistance to PTR race 1. Of these, 88 were also resistance to Stagonospora nodorum blotch (SNB). Data from the Germplasm Resources Information Network (GRIN) showed 28 accessions also had resistance to other key diseases. Resistance gene analog polymorphism (RGAP) marker analysis was used to determine the genetic relationships among the 88 accessions, and wheat accessions with similar growth habit grouped together despite their country of origin.;Genome-wide association study (GWAS) was conducted using 832 diversity arrays technology (DArT)RTM markers to identify QTL associated with resistance to PTR races 1 and 5 in 567 spring wheat landraces. The DArT markers associated with resistance to races 1 and 5 were detected on chromosomes 1D, 2A, 2B, 2D, 4A, 5B, and 7D and on 2D, 6A and 7D, and explained phenotypic variance ranging from 1.3 to 3.1% and 2.2 to 5.9%, respectively. This study demonstrates that AM can be useful approach to identify novel genomic regions involved in resistance to PTR. |
