Thesis (M.S.)--University of California, Berkeley. / Includes bibliographical references (leaves 37-39).

Agriculture is a crucial component of the economy of Texas with millions of pounds of peanuts, cotton, wheat, and corn produced annually. However, Texas agricultural crops are not exempt from pathogens, especially Sclerotinia minor Jagger, which was introduced into Texas approximately 25 years ago. A dramatic increase in S. minor disease incidence in the High Plains of Texas during 2004 provided the basis for this study of the pathogen populations in Texas. To characterize the S. minor populations in Texas, aggressiveness and fungicide sensitivity assays were conducted to assess phenotypic characteristics as well as the use of five microsatellite markers to genotypically characterize the pathogen. A large diversity among the populations was found for the phenotypic characteristics; however, there was no evidence that a genotypically unique, highly aggressive, and fungicide resistant "super pathogen" had been introduced or evolved. The populations of S. minor in Texas were moderately aggressive (26.15% of infected tissue), but there were also isolates found that have the inability to infect peanuts (less than 3% of infected tissue) as well as highly aggressive pathogens with theAll fungicides tested were effective in limiting the growth of the pathogen; however, there were significant differences in the effectiveness of the fungicides. Thiophanate-methyl and dichloran were the least effective fungicides in inhibiting the growth of S. minor while boscalid, iprodione, and fluazinam were the best. Fluazinam exerted the most lasting suppressive effect on pathogen. A positive correlation between aggressiveness and fungicide sensitivity to fluazinam and boscalid was found; therefore, no ecological tradeoff was found when increasing these two phenotypic characteristics. Whereas extensive genotypic diversity (50 unique genotypes) was found in Texas, the predominate pathogen was a clone. Genotype TX1 was a clone that accounted for more than 48% of genotypes in Texas populations, identified in all of the sampled counties. The index of association demonstrated that there was a lack of gene flow occurring in the S. minor populations, therefore confirming that the pathogen reproduced primarily through mycelogenic germination. ability to infect more an 55% of the leaflet surface.

Thesis (Ph. D.)--Washington State University, December 2009. / Title from PDF title page (viewed on Dec. 15, 2009). "Department of Plant Pathology." Includes bibliographical references.

Sclerotinia stem rot (SSR) disease is one of the most devastating diseases of canola in the Canadian prairies caused by the fungus Sclerotinia sclerotiorum (Lib.) de Bary. Yield losses ranging between 5 to 100 percent can be experienced as a result of this disease. This study evaluated the impacts of weather and microclimate on SSR development in canola with varying canopy density. Ascospore dispersal and disease incidence were compared under modified canopy densities and misting regimes to alter microclimate. The effectiveness of crop rotation and the influence of neighbouring non host crops were also analyzed in this study. A randomized complete block design was used to compare values for canopy density, microclimate and disease development under 3 seeding rates and 3 fertilizer treatments. This design was implemented over 4 site-years, in Winnipeg and Carman during 2011 and 2012. Weather stations were installed to monitor environmental conditions at each site and compare these to disease. At each site, a wheat plot was created to examine ascospore release under a non-host crop to determine the influence such a crop may have on neighbouring canola fields. Results of this study showed that peaks in ascospore concentrations occurred simultaneously between Winnipeg and Carman fields during both years indicating that regional weather conditions are important for ascospore release. Disease development in canola fields occurred where adequate precipitation and relative humidity were present prior to ascospore release and dispersal. A decrease in relative humidity and an increase in temperature were required for spore release from apothecia. Disease development was greater in Carman, where relative humidity values overall were higher and temperatures remained lower compared to those in Winnipeg in 2011 and 2012. Ascospore release did occur under the wheat canopy and ascospores were dispersed to a distance of at least 7 meters from the plot.

Thesis (Ph. D.)--University of Adelaide, 1984. / Includes bibliographical references (leaves 128-136).

Thesis (PH. D.)--University of Chicago, 1919. / "Private edition, distributed by the University of Chicago Libraries, Chicago, Illinois, 1920." "Reprinted from the Journal of the American chemical society, Vol. XLII. No. 3. March, 1920." Includes bibliographical references.

Thesis (Ph. D.)--University of Chicago, 1919. / "Private edition, distributed by the University of Chicago Libraries, Chicago, Illinois, 1920." "Reprinted from the Journal of the American chemical society, Vol. XLII. No. 3. March, 1920." Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1972. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M. App. Sc.)--University of Queensland, 2001. / Includes bibliographical references.

Thesis (doctoral)--Swedish University of Agricultural Sciences, 2000. / Includes bibliographical references.