Fusarium head blight (FHB or scab) caused by Fusarium spp. is a destructive disease of wheat. Host resistance coupled with other integrated pest management practices, is considered the best approach to control FHB. In an effort to identify novel sources of FHB resistance, we evaluated wheat germplasm in a Fusarium disease nursery in 2016 and 2017. Four thousand accessions from the Plant Gene Resource of Canada (PGRC), which has a world-wide collection of Triticum aestivum, were evaluated in a field FHB nursery for two seasons; 400 lines with the greatest resistance were selected for genome-wide association study (GWAS) to confirm the new resistance genes. Preliminary GWAS identified novel FHB alleles/or QTLs from the PGRC AM panel: 2 QTLs from chromosomes 2B and 7B for FHB incidence in 2016; 2 QTLs from 1B and 7A for FHB incidence in 2017 and for FHB severity in 2016, 4 QTLs from chromosomes 2B, 4A, 5A and 6A; and from 2017, 8 QTLs from chromosomes 1A, 1B, 2B, 3A, 3D, 5A, 5B and 6A.

In addition, 412 lines were evaluated from a synthetic hexaploid wheat association mapping (SHW AM) panel, which were created by crossing durum wheat (AABB) and Aegilops tauschii (DD) at the International Wheat Research Centre in Mexico (CIMMYT). Thirty-eight SHW consistently showed low incidence and severity (comparable to the resistant check Sumai3) across biological replications and multi-year testing in the field. All 38 lines also had low DON accumulation. Greenhouse evaluation for Type II resistance (disease spread within the spike after point inoculation) of these 38 lines, identified 2 lines with very strong resistance. These lines will be useful in the development of FHB-resistant wheat germplasm and populations for discovery of novel FHB resistance. The SHW AM panel was genotyped with wheat 90K Infinium SNP chips. A high density haplotype map was developed with markers identified by anchoring to the bread wheat consensus map. With genotypic and phenotypic data, we performed GWAS analysis and identified 4 QTLs from chromosomes 2A, 5D, 7B and 7D for FHB incidence in 2016 and 5 QTLs from 1A, 2B, 3B, 5A and 6D in 2017. For FHB severity in 2016, 7 QTLs from chromosomes 1B, 2D, 3A, 3D, 4B, 7A, and 7B were identified, and in 2017, 7 QTLs from chromosomes 2D, 3B, 4D, 5D, 6B, 6D, and 7D were detected.  Seven high priority QTLs including 2A, 2D, 3B, 5A, 5D, 7B and 7D were selected and Kompetitive allele specific PCR (KASPar) markers flanking these QTLs successfully developed for the practise of marker assisted selection (MAS).