Tan spot, caused by the necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr), is a major foliar disease in wheat. QTL mapping and meta-QTL analysis are effective methods to understand genetic basis of tan spot resistance, which can further facilitate resistant variety development. A number of QTL mapping studies have been conducted in hexaploid bread wheat whereas few mapping studies have been carried out in tetraploid wheat. Four interconnected tetraploid wheat mapping populations were evaluated for resistance to race 2 isolate 86-124. Twelve QTL were identified in three of the four mapping populations. To further extend understanding of tan spot resistance, meta-QTL analysis was conducted by using reported QTL from 14 previous QTL mapping studies. Three meta-QTL located on chromosomes 2A, 3B, and 5A showed large genetic effects in multiple populations and conferred resistance to multiple races. Integrating those race-nonspecific QTL could provide high and stable tan spot resistance in wheat.

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Master of Science / Department of Agronomy / Jianming Yu / Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is an economically important foliar disease worldwide. Race 1 of the fungus, which produces the necrosis toxin Ptr ToxA and the chlorosis toxin Ptr ToxC, is the most prevalent race in the Great Plains of the United States. The purposes of this study are to 1) identify and map novel quantitative trait loci (QTL) involved in resistance to tan spot race 1 in common wheat (Triticum aestivum L.) and 2) explore the inverse gene-for-gene interaction in the wheat-P. tritici-repentis pathosystem. A population of 288 F2:6 recombinant inbred lines (RILs) developed from the cross between Chinese landrace WSB (resistant) and Ning7840 (highly susceptible) was firstly used to identify genomic regions harboring novel sources of resistance. Two QTLs associated with resistance to chlorosis were mapped to the short arm of chromosome 1A and 2B in the WSB/Ning7840 population. No interaction was found between the two QTL. To further explore the specific wheat-ToxC model, three other populations were developed based on two susceptible parents, Ning7840 and Wheaton. QTL analysis revealed that common QTL were detected in populations shared with the same susceptible parents. The observations suggested that susceptibility rather than resistance for tan spot chlorosis is specific and presented evidence for the inverse gene-for-gene theory in the WSB-ToxC pathosystem. Leaf rust, caused by Puccinia triticina Eriks., is another important foliar disease of common wheat worldwide. The rust-resistance genes Lr41 and Lr42 from T. tauschii accessions TA2460 (Lr41) and TA2450 (Lr42) have been used as sources of rust resistance in breeding programs. Molecular markers linked to these genes are essential tools for gene pyramiding. Two BC3F2:6 mapping populations were evaluated for leaf rust resistance at both seedling and adult plant stages and analyzed with simple sequence repeat (SSR) markers. Both genetic and physical mapping confirmed that markers linked to Lr41 and Lr42 were on chromosome arm 2DS and 1DS, respectively. Marker analysis in a diverse set of wheat germplasm indicated that tightly linked markers for Lr41 and Lr42 can be used for marker-assisted selection (MAS) in breeding programs.

Master of Science / Department of Plant Pathology / William W. Bockus / The effects of tan spot on lipid profiles in wheat leaves were quantified by mass spectrometry. Inoculation with Pyrenophora tritici-repentis significantly reduced the amount of many lipids, including the major lipids monogalactosyldiacylglycerol (MGDG) and digalactosyldiacylglycerol (DGDG), in leaves over time. These two lipids accounted for 89% of the mass spectral signal of detected lipids in wheat leaves. Reductions in amounts of lipids were at much higher rates over time for susceptible cultivars compared with resistant cultivars. Furthermore, data show that cultivars resistant to tan spot have different lipid profiles when compared with susceptible cultivars. Resistant cultivars had more MGDG and DGDG than susceptible ones, even in non-inoculated leaves. Using linear models that were fit to data, non-inoculated cultivars with a rating of 1 (highly resistant to tan spot) were calculated to have 66.1% more MGDG and 52.7% more DGDG signal than cultivars with a rating of 9 (highly susceptible). These latter findings are indirect evidence that the amounts of some lipids in wheat leaves may be determining factors in the resistance response of cultivars to tan spot.

Doctor of Philosophy / Genetics Interdepartmental Program / Bikram S. Gill / Leaf rust, caused by fungus Puccinia triticina, is an important foliar disease of wheat worldwide. Breeding for race-nonspecific resistant cultivars is the best strategy to combat this disease. Aegilops tauschii, D genome donor of hexaploid wheat, has provided resistance to several pests and pathogens of wheat. To identify potentially new adult plant resistance (APR) genes, 371 geographically diverse Ae. tauschii accessions were evaluated in field with leaf rust (LR) composite culture of predominant races. Accessions from Afghanistan only displayed APR whereas both seedling resistance and APR were common in the Caspian Sea region. Seventeen accessions with high APR were selected for production of synthetic hexaploid wheat (SHW), using ‘TetraPrelude’ and/or ‘TetraThatcher’ as tetraploid parents. Six SHWs were produced and evaluated for APR to LR and resistance to tan spot at seedling stage. Genetic analysis and mapping of APR introgressed from accession TA2474 was investigated in recombinant inbred lines (RIL) population derived from cross between SHW, TA4161-L3 and spring wheat cultivar, ‘WL711’. Genotyping-by-sequencing approach was used to genotype the RILs. Maximum disease severity (MDS) for LR was significantly correlated among all experiments and APR to LR was highly heritable trait in this population. Nine genomic regions significantly associated with APR to LR were QLr.ksu-1AL, QLr.ksu-1BS, QLr.ksu-1BL.1, QLr.ksu-1BL.2, QLr.ksu-2DS, QLr.ksu-2DL, QLr.ksu-5AL, QLr.ksu-5DL and QLr.ksu-6BL. Association of QLr.ksu-1BL.1 with marker Xwmc44 indicated this locus could be slow-rusting APR gene, Lr46/Yr29. QTLs detected on 2DS, 2DL and 5DL were contributed by TA4161-L3 and are novel, along with QLr.ksu-5AL. Tan spot, caused by necrotrophic fungus, Pyrenophora tritici-repentis, has recently emerged as a damaging disease of wheat worldwide. To identify QTLs associated with resistance to Race 1 of P. tritici-repentis, F[subscript]2:3 population derived from cross between SHW, TA4161-L1 and winter wheat cultivar, ‘TAM105’ was used. Two major effect QTLs, QTs.ksu-1AS.1 and QTs.ksu-7AS were significantly associated with tan spot resistance and contributed by TA4161-L1. QTs.ksu-7AS is a novel QTL and explained 17% of the phenotypic variation. Novel QTLs for APR to LR and tan spot identified in SHWs add new variation for broadening the gene pool of wheat and providing resources for breeding of durable resistant cultivars.

Pyrenophora tritici-repentis (Ptr) is the necrotrophic fungus responsible for tan spot of wheat (Triticum aestivum). Ptr causes disease on susceptible wheat cultivars through the production and secretion of host-selective toxins (HSTs). HSTs are compounds that are only known to be produced by fungi and considered to be primary determinants of pathogenicity. Infiltration of these toxins into sensitive wheat elicits the same symptoms as the pathogen, which simplifies investigations of host- pathogen interactions due to exclusion of the pathogen. These characteristics make HSTs ideal molecules to dissect molecular plant-microbe interactions. Known HSTs of Ptr include Ptr ToxA (ToxA), Ptr ToxB (ToxB) and Ptr ToxC (ToxC). ToxA is the most characterized toxin of Ptr, as well as the first proteinaceous HST identified. The proposed mode-of-action for ToxA includes internalization into sensitive wheat mesophyll cells, localization to the chloroplast, photosystem perturbations and elicitation of high amounts of reactive oxygen species (ROS), all of which lead to necrosis. However, it is still unknown how ToxA is transported to the chloroplast. To identify additional interacting components involved in ToxA symptom development, genes were silenced in tobacco plants (Nicotiana benthamiana) using the tobacco rattle virus (TRV) virus-induced gene-silencing (VIGS) system. Four genes were identified that potentially could play a role in ToxA-induced cell death: a 40S ribosomal subunit, peroxisomal glycolate oxidase (GOX), a thiamine biosynthetic enzyme (Thi1), and the R-gene mediator, Sgt1. Ptr exhibits a complex race structure determined by the HST(s) produced and the symptom(s) elicited on sensitive wheat cultivars. Currently, there are eight characterized races and other HSTs and races have been proposed. Isolate SO3 was discovered in southern Oregon and elicits ToxA-like symptoms on a wheat differential set, yet lacks the ToxA gene. The transcriptome of SO3 was sequenced, assembled, and aligned to a ToxA-producing isolate, Pt-1C-BFP, which will aid in the identification of the protein(s) that may be responsible for these ToxA-like symptoms. SO3 contains a set of 497 sequences that were not found in the ToxA-producing isolate Pt-1C-BFP (BFP). These sequences should be further investigated to identify those that encode small secreted proteins (SSPs) and could potentially serve as HSTs and pathogenicity factors of SO3. / Graduation date: 2013