Fusarium head blight of wheat: Mechanisms of resistance in Ning 7840 and identification of QTL from a new source of resistance

Fusarium head blight (FHB), caused by Fusarium spp. and Microdochium nivale is a cereal disease threatening the wheat and barley industries in North America as well as Europe, Asia and South America. FHB causes losses in yield as well as reduced grain quality and contamination with mycotoxins that are a serious danger to the health of humans and animals. Host plant resistance to FHB in wheat is quantitative. To date, few sources have been identified that confer a large amount of resistance to FHB. The most widely recognized and used source of resistance is from the Chinese cultivar 'Sumai 3'. The mechanisms underlying Sumai 3 resistance are not understood. Although Sumai 3 provides a large amount of resistance to spread of FHB within infected spikes, this partial resistance is insufficient to prevent the development of FHB under high disease pressure. Identification and verification of other sources of resistance to FHB is critical to enable breeders to combine sources of resistance for a more effective resistance and to prevent the development of genetic uniformity among elite germplasm. The objectives of this research were twofold: (1) to compare progression of disease in a Sumai 3 derived source of resistance ('Ning 7840') versus a susceptible cultivar according to visual and bioassay techniques, and (2) to map potentially novel quantitative trait loci (QTL) controlling FHB resistance from a wheat line whose parents include a hexaploid wheat artificially synthesized from wheat's progenitor species. The spread of disease in Ning 7840 was compared to a susceptible genotype, 'Norm', for visual symptoms of spread in the spikelets, visual symptoms of spread in the rachis, and the presence of the fungus in the rachis according to a bioassay. For both genotypes, the spread of the fungus in the rachis preceded the development of symptoms in the corresponding spikelets. For Ning 7840, spread of the fungus in the rachis was either greatly restricted or equal to that of the susceptible genotype Norm. Nonetheless, the number of scabby spikelets was smaller in Ning 7840 than Norm. These results reveal that a primary mechanism of Sumai 3 resistance to the spread of scabby spikelets is the prevention of the infection of non-inoculated spikelets from infected rachis tissue. For the identification of QTL for resistance to FHB, a dihaploid (DH) wheat population from a cross of CASS94 and Flycatcher was investigated. One-hundred and eight DH lines were phenotyped in the greenhouse for resistance to spread of FHB, and 130 DH lines were genotyped using simple sequence repeat (SSR) primer pairs. Single marker analysis and composite interval mapping identified the locations of one major QTL for resistance on chromosome arm 2DL, and minor QTL for resistance on chromosome 4A and chromosome arms 5AL and 5DL. These results unequivocally verify reports that a QTL controlling resistance to the spread of scabby spikelets is present on chromosome arm 2DL.