No description available.

Thesis (Ph.D.)--Ohio State University, 2005. / Title from first page of PDF file. Document formatted into pages; contains xxi, 195 p.; also includes graphics. Includes bibliographical references (p. 184-195). Available online via OhioLINK's ETD Center

Net blotch is one of the most devastating diseases of barley (<i>Hordeum vulgare</i> L.) and occurs in two distinct forms, net-type net blotch (NTNB) and spot-type net blotch (STNB), caused by the fungal pathogens <i>Pyrenophora teres</i> f. sp. <i>teres</i> Smedeg. and <i>P</i>. <i>teres</i> f. sp. <i>maculata</i> Smedeg., respectively. Several sources of resistance have been previously reported, however, few barley cultivars with high levels of resistance have been developed from these sources. Efficient utilization of available resistance sources is dependent upon successful characterization of genes governing resistance in each resistant parent. Five net blotch resistant parents and one susceptible parent were crossed to identify novel resistance genes, postulate gene number and mode of inheritance, and conduct linkage mapping of novel genes for net blotch resistance. Results indicate that the highly resistant spring barley lines CIho 2291 and CIho 5098, and the winter barley cultivar Nomini each have single dominant genes for NTNB resistance. Resistance to NTNB in CIho 5098 is controlled by the same dominant gene conferring resistance in Nomini. Resistance to NTNB in CIho 2291 is controlled by one dominant gene which putatively is the same gene conferring resistance in ND B112, but differs from the resistance genes carried by the other parents in this study. An F2 population of 238 individuals derived from a cross between Nomini and the susceptible parent "Hector", and an F2 population of 193 individuals derived from a cross between CIho 2291 and Hector were used to map the genes governing NTNB resistance in Nomini and CIho 2291. The dominant gene governing resistance in Nomini, temporarily designated <i>Rpt-Nomini</i>, was mapped to a 9.2 cM region near the centromere of barley chromosome 6H between the flanking microsatellite markers Bmag0344a (r2=0.70) and Bmag0103a (r2=0.90), which were 6.8 cM and 2.4 cM away from <i>Rpt-Nomini</i>, respectively. The dominant gene governing resistance in CIho 2291, temporarily designated <i>Rpt-CIho2291</i>, was mapped to the distal region of barley chromosome 6H between the flanking microsatellite markers Bmag0173 (r2=0.65) and Bmag0500 (r2=0.26), which were 9.9 cM and 24.4 cM from <i>Rpt-CIho2291</i>, respectively. Previous studies have reported genes governing net blotch resistance in this region; however, allelism tests have not been conducted to determine the relationship between these genes. Identification of the chromosomal location of <i>Rpt-Nomini</i> and <i>Rpt-CIho2291</i> will facilitate future efforts in pyramiding multiple independent genes for net blotch resistance. / Ph. D.

The occurrence of spot type net blotch (Pyrenophora teres f. maculata) and net type net blotch (P. teres f. teres) as well as the occurrence of net blotch mating types has been investigated in Lithuania, Latvia and Estonia. Genetic diversity of barley net blotch isolates from various locations in Lithuania was investigated using ISSR and AFLP markers. The net blotch resistance of 150 spring barley varieties was investigated under artificial and natural infection conditions in the field. / Panaudojant molekulinius žymeklius ištirta tinkliškosios dryžligės patogeno Pyrenophora teres populiacijos genetinė įvairovė, nustatyti P. teres formų ir lytinio dauginimosi tipų sutinkamumas Lietuvoje, Latvijoje ir Estijoje. Lietuvos sąlygomis įvertintas Vakarų Europos ekotipo 150 vasarinių miežių veislių ir linijų jaurumas tinkliškajai dryžligei esant skirtingai pradinei infekcijai.

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.

Pyrenophora semeniperda is a generalist fungal pathogen that occurs primarily on monocot seed hosts. It is in the phylum Ascomycota, which includes both self-compatible (homothallic) and self-incompatible (heterothallic) species. Homothallic fungal species contain complementary mating-type (MAT) idiomorphs in a single unikaryotic strain, while heterothallic strains contain a single MAT idiomorph requiring interaction between strains of complementary mating-types for sexual reproduction to occur. Because the majority of P. semeniperda strains contained either MAT1 or MAT2, this species was provisionally categorized as heterothallic. However, many strains contain both MAT idiomorphs and appear to be homothallic. These results warranted a closer look at the MAT idiomorphs and the structure of the P. semeniperda genome in order to assure accurate characterization of the MAT locus. Additionally, an assessment of the geographic distribution of MAT idiomorphs provides us with insight into the genetic diversity of P. semeniperda and the reproductive strategies that it employs. In this study, we characterized the P. semeniperda MAT locus and assessed the idiomorph distribution of 514 isolates from 25 P. semeniperda populations collected from infected Bromus tectorum (cheatgrass) seeds. Additionally, we used simple sequence repeat (SSR) and MAT idiomorph length polymorphisms to demonstrate the existence of dikaryotic strains and pseudohomothallism in this fungus. We identified a unique variable number tandem repeat (VNTR) within each idiomorph of the MAT locus of P. semeniperda. Presence of the VNTR in all MAT loci analyzed from strains collected in the Intermountain West suggests ancient proliferation of this repeat. The persistence and effectiveness of P. semeniperda strains in the cheatgrass pathosystem depend not only on the density of the fungus in the soil, but also on the genetic heterogeneity of each population. Our study suggests that P. semeniperda genetic diversity is increased both through MAT locus-dependent sexual reproduction and asexually through anastomosis.

Thesis (doctoral)--Swedish University of Agricultural Sciences, 2001. / Thesis statement in Swedish and English abstract inserted. Based on 4 previously prepared or published papers reprinted here. Includes bibliographical references.

Contributing to the success of Bromus tectorum in the Intermountain West may be a mechanism called apparent competition, which occurs when one species increases the pressure of a consumer on a second species. This indirect interaction has been documented only a few times in invasive plant systems, and never in a fungal pathosystem. We examined the effects of the invasive annual Bromus tectorum and predation by the seed pathogen Pyrenophora semeniperda on seedling emergence and survival for two native grasses (Pseudoroegneria spicata and Elymus elymoides), by manipulating B. tectorum densities and P. semeniperda inoculum loads in randomized plots. Identical field studies were conducted in Skull Valley, Utah (xeric site) and Sprague, Washington (mesic site). The addition of inoculum decreased emergence of native grass seedlings at both sites and increased the amount of unemerged native seeds that were killed by P. semeniperda. Higher densities of B. tectorum decreased native grass survival at the mesic site and increased survival at the xeric site probably due to the beneficial effects of B. tectorum litter on soil moisture. At both sites, there were more B. tectorum seeds found in the seed banks in plots with high B. tectorum densities than in low-density plots. This indicates an increase in available prey for P. semeniperda. There was a much lower level of infection in B. tectorum seed bank seeds at the mesic site than at the xeric site. The high level of ungerminated native seeds killed by background levels of P. semeniperda, combined with the increase in available prey for the fungus in high-density B. tectorum plots, shows that apparent competition may play a role, along with direct competition, in the success of B. tectorum. This interaction is important to consider when dealing with control of B. tectorum.

No description available.

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