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.

Continued genetic control of the cereal rusts depends on the availability of effective resistance genes. The wild relatives of wheat (Triticum aestivum L.) constitute a source of such genes. Wheat leaf rust (Puccinia triticina Eriks.) resistant Aegilops neglecta accession 155 was crossed with ‘Chinese Spring’. Resistant progeny were initially backcrossed to Chinese Spring and later to Chinese Spring‐Short (a short‐strawed near‐isogenic line) to develop an addition line. Advanced backcross progeny segregated for a resistance gene (designated Lr62) located on an addition chromosome, as well as a resistant phenotype apparently contributed by dominant complementary genes of the wheat genomes. On its own, Lr62 produced infection type (IT); however, in the presence of the two complementary genes its expression was modified to an intermediate response. The addition chromosome appeared to have homeology with group 3 chromosomes of wheat. While attempting to transfer the resistance through allosyndetic pairing induction to a group 3 wheat chromosome, a spontaneous translocation occurred. Aneuploid and microsatellite analyses showed that the translocation involved wheat chromosome 6A, suggesting that the addition chromosome may also have partial homeology to group 6. Microsatellite and meiotic pairing data suggested the presence of a large segment of foreign chromatin replacing the entire 6AS arm and a proximal part of 6AL. Lr62 was effective against a wide range of South African and western Canadian Puccinia triticina pathotypes. In addition to Lr62, the translocation line, 03M119‐71A, carried a seedling stripe rust resistance gene (designated Yr42) effective against South African pathotypes of P. striiformis The resistance genes can be of significant commercial value, however, it may be necessary to further tailor this fairly big translocation through allosyndetic pairing induction.

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.

Recent reports suggested that the Russian wheat aphid (Diuraphis noxia Mordvilko, RWA) resistance gene Dn5 is located on wheat (Triticum aestivum L.) chromosome arm 7DS rather than on 7DL. A further attempt was therefore made to physically map the gene employing the same source material previously used to describe, name, and map it. It was possible to derive monotelosomic 7DL plants carrying Dn5 on the telosome. Such plants could not be developed for the short arm. The identities of the 7DS and 7DL telosomes were confirmed using mapped microsatellite a‐nd endopeptidase markers and showed unequivocally that Dn5 occurs on 7DL. It appears that use of the wrong Dn5 source material could explain some of the inconsistencies in earlier genetic studies involving this gene. In an attempt to also genetically map Dn5, a doubled haploid (DH) mapping population was derived from the cross PI 294994 × ‘Chinese Spring’ (CS). A single RWA resistance gene, believed to be Dn5, segregated in the population and was mapped together with 12 microsatellite loci and the Ep‐D1 locus. The Dn gene mapped near the centromere on 7DS. However, closer inspection of the data suggested that segregation distortion with opposite effect occurred within two areas of the region that was being mapped. The combined distortion effect rendered the data unreliable and it was not possible to unambiguously determine the chromosome arm on which the Dn gene resides. It appeared that the chromosome 7D proximal regions may be problematic in terms of genetic analysis based on segregation data.