|LEWEIN, MEGAN - Washington State University|
|MURRAY, TIMOTHY - Washington State University|
|JERNIGAN, KENDRA - Washington State University|
|CARTER, AARON - Washington State University|
Submitted to: PLoS ONE
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/17/2018
Publication Date: 4/2/2018
Citation: Lewein, M.J., Murray, T.D., Jernigan, K.L., Garland Campbell, K.A., Carter, A.H. 2018. Genome-wide association mapping for eyespot disease in US Pacific Northwest winter wheat. PLoS One. https://doi.org/10.1371/journal.pone.0194698.
Interpretive Summary: Eyespot is a severe crown disease of winter wheat in cool moist growing environments, including the Pacific Northwest. This project examined the genetic architecture of resistance in two collections of winter wheat breeding lines and cultivars that are adapted to the region. In addition to the previously documented Pch1 and Pch2 genes for resistance, several other chromosomes regions were consistently detected in multiple screening environments. These included loci on chromosomes 2A, 5A, 5B, 7AS, 7B. These results identify molecular markers that can be used to select for resistance to the disease early in the breeding program. These results will enable breeders to use genomic tools to ensure that winter wheat breeding material has at least a moderate amount of resistance and have the potential to reduce fungicide costs in the region.
Technical Abstract: Eyespot, caused by the soil-borne necrotrophic fungi Oculimacula yallundae and O. acuformis, is a disease of major economic significance for wheat, barley and rye. Winter wheat (Triticum aestivum L.) grown in areas of high rainfall and moderate winters in the Pacific Northwest (PNW) is most vulnerable to infection. The objective of this research was to identify novel genomic regions associated with eyespot resistance in winter wheat adapted to the PNW. Two winter wheat panels of 469 and 399 lines were compiled for one of the first genome-wide association studies (GWAS) of eyespot resistance in US winter wheat germplasm. These panels were genotyped with the Infinium 9K and 90K iSelect SNP arrays. Both panels were phenotyped for disease resistance in a two-year field study and in replicated growth chamber trials. Growth chamber trials were used to evaluate the genetic resistance of O. acuformis and O. yallundae species separately. Best linear unbiased predictors (BLUPs) were calculated across all field and growth chamber environments. A total of 73 marker-trait associations (MTAs) were detected on nine different chromosomes (1A, 2A, 2B, 4A, 5A, 5B, 7A, 7B and 7D) that were significantly associated (p-value <0.001) with eyespot resistance in Panel A, and 19 MTAs on nine different chromosomes (1A, 1B, 2A, 2D, 3B, 5A, 5B, 7A, and 7B) in Panel B. The most significant SNPs were associated with Pch1 and Pch2 resistance genes on the long arms of chromosome 7D and 7A. Most of the novel MTAs appeared to have a minor effect on reducing eyespot disease. Nevertheless, eyespot disease scores decreased as the number of resistance alleles increased. Seven SNP markers, significantly associated with reducing eyespot disease across environments and in the absence and presence of Pch1, were identified. These markers were located on chromosomes 2A (IWB8331), 5A (IWB73709), 5B (IWB47298), 7AS (IWB47160), 7B (IWB45005) and two SNPs (Ex_c44379_2509 and IAAV4340) had unknown map positions. The additive effect of the MTAs explained most of the remaining phenotypic variation not accounted for by Pch1 or Pch2. This study provides breeders with adapted germplasm and novel sources of eyespot resistance to be used in the development of superior cultivars with increased eyespot resistance.