Genetic architecture of common bunt resistance in winter wheat using genome-wide association study

Background: Common bunt (caused by Tilletia caries and T. foetida) has been considered as a major disease in wheat (Triticum aestivum) following rust (Puccinia spp.) in the Near East and is economically important in the Great Plains, USA. Despite the fact that it can be easily controlled using seed treatment with fungicides, fungicides often cannot or may not be used in organic and low-input fields. Planting common bunt resistant genotypes is an alternative. Results: To identify resistance genes for Nebraska common bunt race, the global set of differential lines were inoculated. Nine differential lines carrying nine different genes had 0% infected heads and seemed to be resistant to Nebraska race. To understand the genetic basis of the resistance in Nebraska winter wheat, a set of 330 genotypes were inoculated and evaluated under field conditions in two locations. Out of the 330 genotypes, 62 genotypes had different degrees of resistance. Moreover, plant height, chlorophyll content and days to heading were scored in both locations. Using genome-wide association study, 123 SNPs located on fourteen chromosomes were identified to be associated with the resistance. Different degrees of linkage disequilibrium was found among the significant SNPs and they explained 1.00 to 9.00% of the phenotypic variance, indicating the presence of many minor QTLs controlling the resistance. Conclusion: Based on the chromosomal location of some of the known genes, some SNPs may be associated with Bt1, Bt6, Bt11 and Bt12 resistance loci. The remaining significant SNPs may be novel alleles that were not reported previously. Common bunt resistance seems to be an independent trait as no correlation was found between a number of infected heads and chlorophyll content, days to heading or plant height

Association mapping of spot blotch resistance in wild barley

Spot blotch, caused by Cochliobolus sativus, is an important foliar disease of barley. The disease has been controlled for over 40 years through the deployment of cultivars with durable resistance derived from the line NDB112. Pathotypes of C. sativus with virulence for the NDB112 resistance have been detected in Canada; thus, many commercial cultivars are vulnerable to spot blotch epidemics. To increase the diversity of spot blotch resistance in cultivated barley, we evaluated 318 diverse wild barley accessions comprising the Wild Barley Diversity Collection (WBDC) for reaction to C. sativus at the seedling stage and utilized an association mapping (AM) approach to identify and map resistance loci. A high frequency of resistance was found in the WBDC as 95% (302/318) of the accessions exhibited low infection responses. The WBDC was genotyped with 558 Diversity Array Technology (DArT®) and 2,878 single nucleotide polymorphism (SNP) markers and subjected to structure analysis before running the AM procedure. Thirteen QTL for spot blotch resistance were identified with DArT and SNP markers. These QTL were found on chromosomes 1H, 2H, 3H, 5H, and 7H and explained from 2.3 to 3.9% of the phenotypic variance. Nearly half of the identified QTL mapped to chromosome bins where spot blotch resistance loci were previously reported, offering some validation for the AM approach. The other QTL mapped to unique genomic regions and may represent new spot blotch resistance loci. This study demonstrates that AM is an effective technique for identifying and mapping QTL for disease resistance in a wild crop progenitor