RESUMEN
Fusarium head blight (FHB) is a highly destructive fungal disease of wheat to which host resistance is quantitatively inherited and largely influenced by the environment. Resistance to FHB has been associated with taller height and later maturity; however, a further understanding of these relationships is needed. An association mapping panel (AMP) of 192 predominantly Canadian spring wheat was genotyped with the wheat 90K single-nucleotide polymorphism (SNP) array. The AMP was assessed for FHB incidence (INC), severity (SEV) and index (IND), days to anthesis (DTA), and plant height (PLHT) between 2015 and 2017 at three Canadian FHB-inoculated nurseries. Seven multi-environment trial (MET) datasets were deployed in a genome-wide association study (GWAS) using a single-locus mixed linear model (MLM) and a multi-locus random SNP-effect mixed linear model (mrMLM). MLM detected four quantitative trait nucleotides (QTNs) for INC on chromosomes 2D and 3D and for SEV and IND on chromosome 3B. Further, mrMLM identified 291 QTNs: 50 (INC), 72 (SEV), 90 (IND), 41 (DTA), and 38 (PLHT). At two or more environments, 17 QTNs for FHB, DTA, and PLHT were detected. Of these 17, 12 QTNs were pleiotropic for FHB traits, DTA, and PLHT on chromosomes 1A, 1D, 2D, 3B, 5A, 6B, 7A, and 7B; two QTNs for DTA were detected on chromosomes 1B and 7A; and three PLHT QTNs were located on chromosomes 4B and 6B. The 1B DTA QTN and the three pleiotropic QTNs on chromosomes 1A, 3B, and 6B are potentially identical to corresponding quantitative trait loci (QTLs) in durum wheat. Further, the 3B pleiotropic QTN for FHB INC, SEV, and IND co-locates with TraesCS3B02G024900 within the Fhb1 region on chromosome 3B and is ~3 Mb from a cloned Fhb1 candidate gene TaHRC. While the PLHT QTN on chromosome 6B is putatively novel, the 1B DTA QTN co-locates with a disease resistance protein located ~10 Mb from a Flowering Locus T1-like gene TaFT3-B1, and the 7A DTA QTN is ~5 Mb away from a maturity QTL QMat.dms-7A.3 of another study. GWAS and QTN candidate genes enabled the characterization of FHB resistance in relation to DTA and PLHT. This approach should eventually generate additional and reliable trait-specific markers for breeding selection, in addition to providing useful information for FHB trait discovery.
RESUMEN
Gluten strength is one of the factors that determine the end-use quality of durum wheat and is an important breeding target for this crop. To characterize the quantitative trait loci (QTL) controlling gluten strength in Canadian durum wheat cultivars, a population of 162 doubled haploid (DH) lines segregating for gluten strength and derived from cv. Pelissier × cv. Strongfield was used in this study. The DH lines, parents, and controls were grown in 3 years and two seeding dates in each year and gluten strength of grain samples was measured by sodium dodecyl sulfate (SDS)-sedimentation volume (SV). With a genetic map created by genotyping the DH lines using the Illumina Infinium iSelect Wheat 90K SNP (single nucleotide polymorphism) chip, QTL contributing to gluten strength were detected on chromosome 1A, 1B, 2B, and 3A. Two major and stable QTL detected on chromosome 1A (QGlu.spa-1A) and 1B (QGlu.spa-1B.1) explaining 13.7-18.7% and 25.4-40.1% of the gluten strength variability respectively were consistently detected over 3 years, with the trait increasing alleles derived from Strongfield. Putative candidate genes underlying the major QTL were identified. Two novel minor QTL (QGlu.spa-3A.1 and QGlu.spa-3A.2) with the trait increasing allele derived from Pelissier were mapped on chromosome 3A explaining up to 8.9% of the phenotypic variance; another three minor QTL (QGlu.spa-2B.1, QGlu.spa-2B.2, and QGlu.spa-2B.3) located on chromosome 2B explained up to 8.7% of the phenotypic variance with the trait increasing allele derived from Pelissier. QGlu.spa-2B.1 is a new QTL and has not been reported in the literature. Multi-environment analysis revealed genetic (QTL) × environment interaction due to the difference of effect in magnitude rather than the direction of the QTL. Eleven pairs of digenic epistatic QTL were identified, with an epistatic effect between the two major QTL of QGlu.spa-1A and QGlu.spa-1B.1 detected in four out of six environments. The peak SNPs and SNPs flanking the QTL interval of QGlu.spa-1A and QGlu.spa-1B.1 were converted to Kompetitive Allele Specific PCR (KASP) markers, which can be deployed in marker-assisted breeding to increase the efficiency and accuracy of phenotypic selection for gluten strength in durum wheat. The QTL that were expressed consistently across environments are of great importance to maintain the gluten strength of Canadian durum wheat to current market standards during the genetic improvement.