Genome-wide association mapping identifies common bunt (Tilletia caries) resistance loci in bread wheat (Triticum aestivum) accessions of the USDA National Small Grains Collection.

KEY MESSAGE: Association mapping and phenotypic analysis of a diversity panel of 238 bread wheat accessions highlights differences in resistance against common vs. dwarf bunt and identifies genotypes valuable for bi-parental crosses. Common bunt caused by Tilletia caries and T. laevis was successfully controlled by seed dressings with systemic fungicides for decades, but has become a renewed threat to wheat yield and quality in organic agriculture where such treatments are forbidden. As the most efficient way to address this problem is the use of resistant cultivars, this study aims to broaden the spectrum of resistance sources available for breeders by identifying resistance loci against common bunt in bread wheat accessions of the USDA National Small Grains Collection. We conducted three years of artificially inoculated field trials to assess common bunt infection levels in a diversity panel comprising 238 wheat accessions for which data on resistance against the closely related pathogen Tilletia controversa causing dwarf bunt was already available. Resistance levels against common bunt were higher compared to dwarf bunt with 99 accessions showing [Formula: see text] 1% incidence. Genome-wide association mapping identified six markers significantly associated with common bunt incidence in regions already known to confer resistance on chromosomes 1A and 1B and novel loci on 2B and 7A. Our results show that resistance against common and dwarf bunt is not necessarily controlled by the same loci but we identified twenty accessions with high resistance against both diseases. These represent valuable new resources for research and breeding programs since several bunt races have already been reported to overcome known resistance genes.

Fine-mapping of the Fusarium head blight resistance QTL Qfhs.ifa-5A identifies two resistance QTL associated with anther extrusion.

KEY MESSAGE: Fine-mapping separated Qfhs.ifa-5A into a major QTL mapping across the centromere and a minor effect QTL positioned at the distal half of 5AS. Both increase Fusarium resistance and anther extrusion. The Fusarium head blight (FHB) resistance QTL Qfhs.ifa-5A resides in the low-recombinogenic pericentromeric region of chromosome 5A making fine-mapping particularly arduous. Qfhs.ifa-5A primarily contributes resistance to fungal entry with the favorable allele descending from the highly Fusarium resistant cultivar Sumai-3. Fine-mapping a near-isogenic recombinant inbred line population partitioned the Qfhs.ifa-5A interval into 12 bins. Near-isogenic lines recombining at the interval were phenotyped for FHB severity, anther retention and plant height. Composite interval mapping separated the initially single QTL into two QTL. The major effect QTL Qfhs.ifa-5Ac mapped across the centromere and the smaller effect QTL Qfhs.ifa-5AS mapped to the distal half of 5AS. Although Qfhs.ifa-5Ac and Qfhs.ifa-5AS intervals were as small as 0.1 and 0.2 cM, their corresponding physical distances were large, comprising 44.1 Mbp and 49.2 Mbp, respectively. Sumai-3 alleles at either QTL improved FHB resistance and increased anther extrusion suggesting a pleiotropic effect of anthers on resistance. This hypothesis was supported by greenhouse experiments using the susceptible cultivar Remus and its resistant near-isogenic line NIL3 carrying the entire Qfhs.ifa-5A segment. By manually removing anthers prior to spray inoculation both, Remus and NIL3 became almost equally resistant in the early phase of the disease development and were significantly less diseased than variants without anther manipulation. At late time points the positive effect of the anther removal became smaller for Remus and disappeared completely for NIL3. Results affirm that absence of anthers enhanced resistance to initial infection but did not protect plants from fungal spreading within spikes.