Dwayne HegedusGeorge Khachatourians2011-04-152013-01-042012-04-212013-01-042011-042011-04-01April 2011http://hdl.handle.net/10388/etd-04152011-115612S. sclerotiorum has been studied for over 100 years. Despite this, a definite resistance mechanism to this plant pathogen remains to be identified. Researchers continue to examine the S. sclerotiorum life cycle to identify stages where effective disease management strategies can be applied. The development of molecular tools has allowed for a better understanding of the pathogen and created new opportunities for research on plant-pathogen interactions. Most of the past research on pathogenicity factors produced by this pathogen, such as hydrolytic enzymes, studied them in isolation. This thesis examines how S. sclerotiorum pathogenicity factors, including cutinases, polygalacturonases and necrosis-inducing peptides, work in concert during the infection. The first study explored processes for cuticle penetration leading to the identification of the gene encoding S. sclerotiorum cutinase A and the characterization of the factors that govern its expression during the infection. The second study investigated how the pathogen penetrates the cell wall and proliferates within the host. In this regard, the mechanism with which expression of S. sclerotiorum polygalacturonase genes is regulated was elucidated. The interplay with host polygalacturonase inhibitor proteins was also demonstrated and related to the mechanisms of host resistance. The third study examined factors involved in tissue necrosis and two necrosis-inducing proteins were characterized. This study also unraveled part of the signaling mechanisms that allow for the pathogen to regulate pathogenicity gene expression during the infection. The signaling mechanisms were found to involve calcium, cAMP and at least one S. sclerotiorum mitogen activated protein kinase (SMK3) working in concert to coordinate the infection process. SMK3 was found to play a major role in a variety of vital functions, such as mycelial branching, infection cushion formation and sclerotia production. Genetic transformation of S. sclerotiorum was required to enable certain aspects of this study. My approach to this led to the development of a highly efficient method to isolate homokaryotic lines of filamentous fungi. In conclusion, this thesis has advanced the understanding of S. sclerotiorum-host interactions and identified a number of factors involved in pathogenesis.en-USPolygalacturonase inhibitor proteinNecrosis inducing proteinMAPKPolygalacturonaseSignallingPathoginicityCutinasetext