A diallel study to detect genetic background variation for FHB resistance in winter wheat.

Breeding for resistance to Fusarium head blight (FHB) relies strongly on a limited number of larger-effect resistance QTL that have been mapped and associated with nearby markers. Smaller-effect (background) resistance QTL may also contribute moderate levels of resistance yet are mostly poorly characterized. Overall resistance of a genotype is determined by the combined action of both types of resistance QTL. This study aimed to identify well-adapted, advanced hard red winter (HRW) wheat breeding lines with useful background resistance QTL. A diallel trial consisting of 11 parents and 55 non-reciprocal F1 hybrids was tested for Type II FHB resistance in a replicated greenhouse experiment. Significant differences were detected among entries for disease severity (DS), general combining ability (GCA) and specific combining ability (SCA) with four parents being identified as the best general combiners with lowest DS. The ratio of GCA:SCA effects suggested that additive QTL effects were of primary importance. Overall, resistance QTL showed incomplete dominance, an excess of dominant alleles, and a greater contribution of positive effect genes. F2 of the six best F1 hybrids with the lowest DS were compared in a second greenhouse FHB trial to select possible transgressive segregates for continued evaluation and line development.

The use of PI 277012-derived Fusarium head blight resistance QTL in winter wheat breeding.

Fusarium head blight (FHB) caused by Fusarium graminearum results in substantial grain yield and quality losses in common wheat (Triticum aestivum L.). Genetic resistance is partial but crucial for effective, integrated management of the disease. Host resistance is conditioned by numerous small effect quantitative trait loci (QTL) that are strongly affected by the environment and genetic background. Qfhb.rwg-5A.1 and Qfhb.rwg-5A.2 (PI 277012 is the source for both genes) are two recently discovered FHB resistance QTL that also occur in spring wheat GP80 (PI 277012 derivative). To transfer the PI 277012 resistance from GP80 to hard winter wheat (HWW), GP80 was first crossed with Novus-4. The F1 hybrid was crossed with SY Monument, following which marker-selected progeny were crossed with, and backcrossed to, ND Noreen. To potential carriers of FHB resistance QTL among the 22 F1 of the ND Noreen cross, simple sequence repeat (SSR) markers, Illumina 90 K single nucleotide polymorphism (SNP) haplotypes and greenhouse FHB Type II resistance tests were done. Likely homozygotes for Qfhb.rwg.5A.1 and Qfhb.rwg.5A.2, were selected and backcrossed to ND Noreen. In the B1F1, 131 plants were evaluated for SNP haplotypes, SSR markers and FHB resistance. Nine B1F2:3 lines were derived, and their resistance confirmed in a third greenhouse FHB trial. The results suggested that eight lines had higher resistance and were comparable to GP80 with the Qfhb.rwg-5A.2 markers occurring in all eight and the Qfhb.rwg-5A.1 markers occurring in four lines. The eight selections constitute a valuable HWW resistance breeding resource.

Characterization of recombinants of the Aegilops peregrina-derived Lr59 translocation of common wheat.

KEY MESSAGE: A compensating, recombined Lr59 translocation with greatly reduced alien chromatin was identified. Microsatellite locus Xdupw217 occurs within the remaining segment and can be used as a co-dominant marker for Lr59. In earlier studies, leaf rust (caused by Puccinia triticina Eriks.) resistance gene Lr59 was transferred from Aegilops peregrina (Hackel) Maire et Weiler to chromosome arm 1AL of common wheat (Triticum aestivum L.). The resistance gene was then genetically mapped on the translocated chromosome segment following homoeologous pairing induction. Eight recombinants that retained the least alien chromatin apparently resulted from crossover within a terminal region of the translocation that was structurally different from 1AL. These recombinants could not be differentiated by size, and it was not clear whether they were compensating in nature. The present study determined that the distal part of the original translocation has group 6 chromosome homoeology and a 6BS telomere (with the constitution of the full translocation chromosome being 1AS·1L(P)·6S(P) ·6BS). During the allosyndetic pairing induction experiment to map and shorten the full size translocation, a low frequency of quadrivalents involving 1A, the 1A translocation, and two 6B chromosomes was likely formed. Crossover within such quadrivalents apparently produced comparatively small compensating alien chromatin inserts within the 6BS satellite region on chromosome 6B of seven of the eight recombinants. It appears that the Gli-B2 storage protein locus on 6BS has not been affected by the recombination events, and the translocations are therefore not expected to affect baking quality. Simple sequence repeat marker results showed that Lr59-151 is the shortest recombinant, and it will therefore be used in breeding. Marker DUPW217 detects a homoeo-allele within the remaining alien chromatin that can be used for marker-assisted selection of Lr59.

Evaluation and Association Mapping of Resistance to Tan Spot and Stagonospora Nodorum Blotch in Adapted Winter Wheat Germplasm.

Tan spot and Stagonospora nodorum blotch (SNB), often occurring together, are two economically significant diseases of wheat in the Northern Great Plains of the United States. They are caused by the fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively, both of which produce multiple necrotrophic effectors (NE) to cause disease. In this work, 120 hard red winter wheat (HRWW) cultivars or elite lines, mostly from the United States, were evaluated in the greenhouse for their reactions to the two diseases as well as NE produced by the two pathogens. One P. nodorum isolate (Sn4) and four Pyrenophora tritici-repentis isolates (Pti2, 331-9, DW5, and AR CrossB10) were used separately in the disease evaluations. NE sensitivity evaluation included ToxA, Ptr ToxB, SnTox1, and SnTox3. The numbers of lines that were rated highly resistant to individual isolates ranged from 11 (9%) to 30 (25%) but only six lines (5%) were highly resistant to all isolates, indicating limited sources of resistance to both diseases in the U.S. adapted HRWW germplasm. Sensitivity to ToxA was identified in 83 (69%) of the lines and significantly correlated with disease caused by Sn4 and Pti2, whereas sensitivity to other NE was present at much lower frequency and had no significant association with disease. As expected, association mapping located ToxA and SnTox3 sensitivity to chromosome arm 5BL and 5BS, respectively. A total of 24 potential quantitative trait loci was identified with -log (P value) > 3.0 on 12 chromosomes, some of which are novel. This work provides valuable information and tools for HRWW production and breeding in the Northern Great Plains.