v, 105 leaves : ill. ; 25 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--Dept. of Plant Pathology, Waite Agricultural Research Institute, University of Adelaide, 1973

Thesis (Ph. D.)--University of Wisconsin--Madison, 1956. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 89-93).

Thesis (M.S.)--University of Wisconsin--Madison. / Typescript. Includes bibliographical references (leaves 234-258).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1959. / Typescript. Abstracted in Dissertation abstracts, v. 19 (1959) no. 8, p. 1884-1885. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 88-93).

Thesis (M.S.)--University of Wisconsin--Madison. / Typescript. Title from title screen (viewed Oct. 1, 2007). Includes bibliographical references (leaves 234-258). Online version of the print original.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1956. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 51-52).

No description available.

No description available.

The fungus Ceratocystis fagacearum (Bretz) Hunt causes the vascular disease of oak wilt and has been decimating live oaks (Quercus virginiana Mill. and Quercus fusiformis Small.) and red oaks (Quercus texana Small and Quercus marilandica Muenchh.) in Texas. The purpose of this research was to test the hypotheses that live oaks have heritable tolerance to oak wilt, and that allozyme markers are associated with this tolerance. One-year-old half-sib and two-year-old clonal progeny of live oaks (Q. fusiformis) were grown from acorns and ramets from a disease center and then challenged with C. fagacearum. Allozyme analyses were used to compare the pre- and post-epidemic populations in two natural disease centers to search for alleles associated with survivability and decreased crown loss. Half-sib and clonal challenge tests supported the hypothesis that heritable tolerance to the pathogen occurs in live oaks. The progeny tolerances seen in half-sib and clonal groups did not correlate with parental tree performance. This finding suggests that the tolerance of one-year-old seedlings in the greenhouse setting is not a good predictor of how mature trees will do in a natural setting. Seedlings may not be a good model for testing tolerance to a pathogen. The ability to survive this vascular pathogen is containment, and seedlings may be too small to test this type of tolerance. The clonal groups from post-epidemic trees performed better than the seedlings. They may have an increased resistance because they are mature or they may have a postdisease immunity. No significant allele frequencies between pre- and post-epidemic trees were consistent among sites or with previous research. The different disease sites had remarkably similar allele frequencies which indicate high levels of gene flow among sites. Both sites were found to contain significant numbers of clones, but the Izoro site had significantly larger clonal groups. Sites were in Hardy-Weinberg equilibrium which indicates substantial sexual reproduction and not just clonal reproduction is taking place. Several cases of linkage disequilibrium occurred at the Izoro site, but population structure was responsible in all but one case.

Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.