Stagonospora nodorum is a necrotrophic fungal pathogen that is the causal agent of leaf and glume blotch on wheat. Very little is currently known about the molecular mechanisms required for pathogenicity of S. nodorum, despite its major impact on Australian agriculture. S. nodorum is a polycyclic pathogen. Rain-splashed pycnidiospores attach to and colonise wheat tissue and subsequently sporulate within 2-3 weeks. Several cycles of infection are needed to build up inoculum for the damaging infection of flag leaves and heads, sporulation is therefore a critical component of the infection cycle of S. nodorum; our aim is to determine the genetic and biochemical requirements for sporulation for development of control of the pathogen. Disease progression of S. nodorum on wheat cv. Amery was monitored by light microscopy to determine the time point when pycnidia development began. Early pycnidia development was evident 12 days post-infection. This information was used to guide a genomics and a metabolomics based approach to determine the requirements for sporulation in S. nodorum. The genomics approach utilised two cDNA libraries created from sporulating and non-sporulating cultures. EST frequency was used to determine highly expressed genes under the two developmental states. Gene expression from the most highly represented genes during sporulation were confirmed using quantitative PCR. A gene encoding an arabitol 4-dehydrogenase (Abd1), was mutagenised, in its absence sporulation was reduced by approximately 20%. The metabolomics approach isolated metabolites from both in planta infection and in vitro growth. Rapid changes in the abundance of metabolites were detected during the onset of sporulation. Key fungal metabolites identified include mannitol and trehalose. The concentration of both mannitol and trehalose increased dramatically in concert with pycnidia formation. Both mannitol and trehalose have also been linked to pathogenicity in filamentous fungi. Creation of deletion mutants of the gene encoding trehalose 6-phosphate synthase showed the synthesis of trehalose is required for full sporulation of S. nodorum in planta and in vitro.

Thesis (M.S.)--Worcester Polytechnic Institute. / Keywords: Turnip crinkle virus; Hypersensitive response. Includes bibliographical references (leaves 52-61).

Thesis (Ph.D.) -- Flinders University, Dept. of Medical Biotechnology. / Typescript (bound). Includes bibliographical references (leaves 256 - 283). Also available online.

Thesis (Ph. D.)--Ohio State University, 2008.

Thesis (Ph.D.)--University of Missouri-Columbia, 2006. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on May 1, 2009) Vita. Includes bibliographical references.

Thesis (Ph.D.)(Microbiology))--University of Pretoria, 2004. / Summary in English. Includes bibliographical references.

Thesis (Ph.D.)--University of Delaware, 2008. / Principal faculty advisors: Jack B. Gingrich and Douglas W. Tallamy, Dept. of Entomology & Wildlife Ecology. Includes bibliographical references.

Thesis (Ph.D.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on March 12, 2009) Includes bibliographical references.

Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.

The filamentous fungus Magnaporthe oryzae is a devastating pathogen of cultivated rice. M. oryzae elaborates a pressurized dome-shaped infection structure, called the appressorium, which physically ruptures the cuticle and gains entry into host tissue. Intracellular invasive hyphae invade neighbouring host cells through plasmodesmata. The Pmk1 MAPK cascade is well known for its roles in regulating the formation and function of the appressorium. Interestingly, ∆pmk1 mutants cannot infect host plant tissue through wounds, suggesting a role in invasive growth. Here, I define biological functions of the Pmk1 MAPK at various stages of the life cycle, by using a controllable version of Pmk1 that is specifically inhibited by a cell-permeable compound without disturbing other wild-type kinases. The Pmk1 MAPK signalling regulates morphogenesis of narrow invasive hyphae traversing the host cell wall, and modulates production of several putative secreted effectors, providing a direct link between the signalling cascade and effector-driven host immune suppression. These results indicate that the Pmk1 pathway is a central regulator of infection-related development necessary for many stages of plant infection including appressorium development, plant penetration, and importantly tissue colonisation. I also report the role of cell cycle progression in the development of plant infection structure. By using two novel conditional mutants that arrest in S and G2 phases, I defined that S-phase progression is crucial for appressorium-mediated plant penetration.