Thesis (M.S.)--West Virginia University, 2004. / Title from document title page. Document formatted into pages; contains viii, 72 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 65-67).

Presented as Thesis (Ph. D.)--University of Wisconsin--Madison, 1918. / Cover title. Reprinted from Journal of agricultural research, vol. XIX, no. 4 (15 May 1920). Includes bibliographical references (p. 172).

Presented as Thesis (Ph. D.)--University of Wisconsin--Madison, 1926. / Cover title. Reprinted from Phytopathology, vol. XVI, no. 10 (Oct. 1926). Includes bibliographical references (p. 695-696).

Thesis (M.Inst.Agrar.)(Microbiology)--University of Pretoria, 2005. / Title from opening screen (viewed March 20, 2006). Includes summary. Includes bibliographical references.

Fusarium Ear Blight is a devastating fungal disease of cereals and due to the contamination of the harvested grain with a range of trichothecene mycotoxins presents a risk to human and animal health. The re-emergence of Fusarium graminearum on wheat and maize, the evolution of more aggressive fungal strains and the lack of an effective control strategy, has increased the need for a greater understanding of the disease aetiology. This project aimed to enhance the understanding of the interaction between F. graminearum and wheat (Triticum aestivum), through the utilisation of microscopy and molecular pathogenomics. A detailed investigation of the infection process revealed a prolonged latent period of intercellular infection that preceded host cell death, intracellular colonisation and the onset of disease symptoms. Phenotypic differences in colonisation and mycotoxin gene expression implied that hyphae within the two phases of infection were transcriptionally distinct, while a bioinformatic analysis described the fungal secretome. The two fungal gene-deficient strains assessed, top1 and tri5, were unable to establish symptomless infection or spread throughout the wheat ear, in the presence or absence of mycotoxin production, suggesting the existence of additional virulence factors. Subsequently, a genome wide transcriptome investigation of the two phases of infection, using both Affymetrix and RNA-sequencing technologies, revealed the unique expression profile, and secretome, of the advancing hyphal front of the symptomless infections. This greater understanding of the biphasic interaction will provide a benchmark for comparison with the single gene deficient strains. Finally, a laser capture microdissection procedure was developed to enable future cell-type specific transcriptome experiments. Collectively, I have discovered and developed a model of how F. graminearum establishes symptomless and symptomatic infection. In doing so, this study has enhanced the understanding of this non-biotrophic pathosystem, providing many new lines of investigation, which could greatly improve crop protection strategies.

Thesis (M.Sc.)(Microbiology)--University of Pretoria, 2005. / Title from opening screen (viewed March 28, 2006). Includes summary. Includes bibliographical references.

Thesis (M.S.)--Oregon State University, 2007. / Printout. Includes bibliographical references (leaves 127-141). Also available on the World Wide Web.

In 1908, Sackett described for the first time what appeared to be a new bacterial disease of alfalfa in Colorado. To this particular disease he applied the name “stem blight" and attributed the cause to a bacterium, Pseudomonas medicaginis. For some two decades or more Sackett's work on this disease was accepted. During this time stem blight, which was first thought to be indigenous to the western United State, was reported from nine states east of the Rocky Mountains. In 1933, Johnson and Valleau described a disease of alfalfa, characterized by stem lesions very similar in appearance to those of stem blight as described by Sackett. These authors determined the cause of this new disease to be a fungus" Phoma medicaginis Malbr. and Roum., and gave to it the name "black stem". Richards in 1934" in reporting on the resistance of certain alfalfa varieties to stem blight in Utah, states in a foot note that a species of Phoma was isolated with considerable uniformity from bacterial stem blight lesions. This author raises the question as to the possible dual etiology of stem blight in Utah. Research work by Remsberg and Hungerford in Idaho, more definitely suggested this dual etiology of' the stem blight complex. These authors determined the black stem lesions on alfalfa to be caused by Phoma medicaginis, and indicated that the darker lesions caused by this fungus were distinct from the lighter colored lesions characteristic of the bacterial stem blight described by Sackett. Because of the similarity of the late stage of bacterial stem blight to the insipient stage of black stem, much confusion has arisen as to their identity and etiology It has been the policy in Utah during recent years to refer to this wide range of stem lesions as stem blight, recognizing that the exact nature and etiology is not known. This disease complex presents a problem in Utah of major economic importance. It is the purpose of this thesis to bring together the known facts regarding stem blight; to determine the specific etiology of the stem blight lesions on alfalfa as they occur in Utah, and if possible to establish definite criteria by which the components of the stem blight complex might be separated.

Abscisic acid (ABA) has been well defined as an important stress hormone in plants. The signaling pathway of ABA involves a family of pyrabactin resistant-like-1 PYR/PYL/RCAR receptors (PYL receptors) that bind ABA and form a complex with a protein phosphatase 2C (PP2C) family member resulting in downstream signaling events. The ABA receptor family has been well characterized in the model dicot Arabidopsis thaliana and more recently this characterization has branched out into cereals Oryza sativa (rice) and Hordeum vulgare (barley), as well as the monocot model plant Brachypodium distachyon and Fragaria vesca (strawberry). The analysis of these characterized ABA receptors and the use of online databases has allowed the identification of multiple putative ABA receptors in Triticum aestivum (wheat). ABA has been historically called a positive effector. Overexpression of proteins in the ABA signalling pathway or exogenous application of ABA is known to cause an increase in drought, cold, and salt tolerance. More recently ABA has been linked to increased fungal susceptibility in several plants. The role ABA plays in the biotic stress response is still largely unexplored. The focus of this project was to identify and characterize a putative wheat ABA receptor through bioinformatics and an in vitro enzyme activity assay, and use virus induced gene silencing (VIGS) to test what role this receptor plays in fugal susceptibility. A total of 13 putative ABA receptors were located, nine of which are unique between the wheat subgenomes. One receptor TaPYL5.1 was recombinantly expressed, purified, and confirmed as an ABA receptor through a phosphatase based enzyme activity assay. A receptor with high sequence identity to TaPYL5.1, TaPYL5.2A, was targeted for plant trials because the TaPYL5.1 plasmid sequence was codon optimized. A VIGS approach was used to knock down TaPYL5.2A in planta. The TaPYL5.2A knockdown plants were found to have an increased resistance to Fusarium Head Blight progression in the early stages of the disease. In conclusion, wheat ABA receptors were successfully identified and an important correlation between decreased receptor levels and increased early Fusarium Head Blight resistance was found. This correlation however was not easily reproducible due to the severity of coupling VIGS with Fusarium Head Blight, and should be followed up with additional studies looking at the broader family of wheat ABA receptors.

published_or_final_version / Ecology and Biodiversity / Doctoral / Doctor of Philosophy