Inverse gene-for-gene interactions contribute additively to tan spot susceptibility in wheat.

KEY MESSAGE: Tan spot susceptibility is conferred by multiple interactions of necrotrophic effector and host sensitivity genes. Tan spot of wheat, caused by Pyrenophora tritici-repentis, is an important disease in almost all wheat-growing areas of the world. The disease system is known to involve at least three fungal-produced necrotrophic effectors (NEs) that interact with the corresponding host sensitivity (S) genes in an inverse gene-for-gene manner to induce disease. However, it is unknown if the effects of these NE-S gene interactions contribute additively to the development of tan spot. In this work, we conducted disease evaluations using different races and quantitative trait loci (QTL) analysis in a wheat recombinant inbred line (RIL) population derived from a cross between two susceptible genotypes, LMPG-6 and PI 626573. The two parental lines each harbored a single known NE sensitivity gene with LMPG-6 having the Ptr ToxC sensitivity gene Tsc1 and PI 626573 having the Ptr ToxA sensitivity gene Tsn1. Transgressive segregation was observed in the population for all races. QTL mapping revealed that both loci (Tsn1 and Tsc1) were significantly associated with susceptibility to race 1 isolates, which produce both Ptr ToxA and Ptr ToxC, and the two genes contributed additively to tan spot susceptibility. For isolates of races 2 and 3, which produce only Ptr ToxA and Ptr ToxC, only Tsn1 and Tsc1 were associated with tan spot susceptibility, respectively. This work clearly demonstrates that tan spot susceptibility in this population is due primarily to two NE-S interactions. Breeders should remove both sensitivity genes from wheat lines to obtain high levels of tan spot resistance.

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.

Pathogenic and genetic diversity of Xanthomonas translucens pv. undulosa in North Dakota.

Bacterial leaf streak (BLS), caused by Xanthomonas translucens pv. undulosa, has become more prevalent recently in North Dakota and neighboring states. From five locations in North Dakota, 226 strains of X. translucens pv. undulosa were collected and evaluated for pathogenicity and then selected strains were inoculated on a set of 12 wheat cultivars and other cereal hosts. The genetic diversity of all strains was determined using repetitive sequence-based polymerase chain reaction (rep-PCR) and insertion sequence-based (IS)-PCR. Bacterial strains were pathogenic on wheat and barley but symptom severity was greatest on wheat. Strains varied greatly in aggressiveness, and wheat cultivars also showed differential responses to several strains. The 16S ribosomal DNA sequences of the strains were identical, and distinct from those of the other Xanthomonas pathovars. Combined rep-PCR and IS-PCR data produced 213 haplotypes. Similar haplotypes were detected in more than one location. Although diversity was greatest (≈92%) among individuals within a location, statistically significant (P ≤ 0.001 or 0.05) genetic differentiation among locations was estimated, indicating geographic differentiation between pathogen populations. The results of this study provide information on the pathogen diversity in North Dakota, which will be useful to better identify and characterize resistant germplasm.

Association mapping of quantitative resistance to Phaeosphaeria nodorum in spring wheat landraces from the USDA National Small Grains Collection.

Stagonospora nodorum blotch (SNB), caused by Phaeosphaeria nodorum, is a destructive disease of wheat (Triticum aestivum) found throughout the United States. Host resistance is the only economically feasible option for managing the disease; however, few SNB-resistant wheat cultivars are known to exist. In this study, we report findings from an association mapping (AM) of resistance to P. nodorum in 567 spring wheat landraces of diverse geographic origin. The accessions were evaluated for seedling resistance to P. nodorum in a greenhouse. Phenotypic data and 625 polymorphic diversity array technology (DArT) markers have been used for linkage disequilibrium (LD) and association analyses. The results showed that seven DArT markers on five chromosomes (2D, 3B, 5B, 6A, and 7A) were significantly associated with resistance to P. nodorum. Genetic regions on 2D, 3B, and 5B correspond to previously mapped quantitative trait loci (QTL) conferring resistance to P. nodorum whereas the remaining QTL appeared to be novel. These results demonstrate that the use of AM is an effective method for identifying new genomic regions associated with resistance to P. nodorum in spring wheat landraces. Additionally, the novel resistance found in this study could be useful in wheat breeding aimed at controlling SNB.

Quantitative trait locus mapping of increased Fusarium head blight susceptibility associated with a wild emmer wheat chromosome.

Chromosome 2A of wild emmer wheat (Triticum turgidum var. dicoccoides) genotype Israel A increases Fusarium head blight (FHB) severity when present in durum wheat (T. turgidum var. durum) cv. Langdon (LDN). The goal of this study was to identify regions of Israel A chromosome 2A associated with this difference in resistance. A recombinant inbred chromosome line population (RICL) from a cross between LDN and the LDN-Israel A chromosome 2A substitution line [LDN(DIC-2A)] was employed for analysis. Three greenhouse FHB evaluations were completed on the RICL to obtain phenotypic data on variation for FHB resistance, and a simple sequence repeat (SSR)-based molecular map of chromosome 2A was developed. Quantitative trait locus (QTL) mapping identified a region on the long arm of chromosome 2A that was associated with FHB resistance in each independent FHB evaluation. Depending on the evaluation, the single best SSR marker in this region accounted for between 21 and 26% of the variation for FHB resistance, with the Israel A marker alleles associated with increased FHB susceptibility. The single best markers from each evaluation reside within an interval of approximately 22 cM. This study identifies one or more new QTL on chromosome 2A in tetraploid wheat that can contribute to significant variation in FHB resistance.

Reaction of Soybean Cultivars to Isolates of Fusarium solani from the Red River Valley.

Five isolates of Fusarium solani, originally isolated from diseased soybean roots in the Red River Valley (RRV) of Minnesota and North Dakota, were evaluated for their ability to cause symptoms on 10 genetically diverse soybean cultivars. Taproots of 2-week-old plants were inoculated with F. solani-infested oat kernels, and 3 and 10 weeks later, plants were evaluated for root rot and foliar symptoms. At 3 weeks after inoculation, taproots of all cultivars had extensive reddish brown to black lesions; root rot severity (1-6 scale) ranged from 4.8 to 5.1, and 3.5% of the plants had died. Foliar symptoms were not observed. At 10 weeks after inoculation, all cultivars showed extensive decay of taproots and >50% of lateral roots were necrotic; root rot severity (1-4 scale) ranged from 2.7 to 3.7, and 42.5% of the plants had died. Foliar symptoms were first observed between the R-1 to R-6 growth stages (about 5 weeks after inoculation) on the lower leaves and consisted of chlorosis at the margins that progressed inward. Veins initially were green, but leaves eventually became chlorotic, then necrotic, and fell with petioles still attached to the stem. In some cases, all of the foliage died. There was no significant (P = 0.05) isolate × cultivar interaction for root rot at 3 or 10 weeks after inoculation or for severity of foliar symptoms. Thirty-three cultivars commonly grown in southern Minnesota and the RRV were evaluated for reaction to one isolate of F. solani. Root rot severity ranged from 4.2 to 5.7 (1-6 scale) and 3.5 to 4.0 (1-4 scale), at 3 and 9 weeks after inoculation, respectively, and >50% of the plants died by 9 weeks after inoculation. Severity of foliar symptoms was low. These results indicate that isolates of F. solani from the RRV cause root rot and foliar symptoms on soybean and that cultivars grown in the region lack resistance to this pathogen. Foliar symptoms were not identical to those associated with sudden death syndrome.