| In this dissertation, I explore the virulence strategy of Pectobacterium carotovorum, a plant pathogen that causes soft rot disease. P. carotovorum infects a wide range of plants, including carrots, beets, and potatoes, and is a significant threat to crop production around the world, causing millions of dollars worth of crop loss each year. In this dissertation, I work with an isolate of P. carotovorum from the irrigation pond of a potato farm experiencing a soft rot outbreak in Wisconsin, U.S.A. In ideal conditions, P. catorovorum can infect the tubers, stems and leafs of a potato plant. P. carotovorum causes disease in part by secreting an array of enzymes that degrade plant cell walls, which causes the characteristic rotting. However, P. carotovorum spends a significant part of its life-history in: soil; on invertebrates that feed on crops; and in both surface and ground water, such as the irrigation pond. Additionally, P. carotovorum possess a variety of other virulence factors required for plant infection, including a Type III secretion system (T3SS). Type III secretion systems allow a pathogen to deliver virulence factors, called effectors, directly into host cells where they can manipulate plant defense responses. The goal of this dissertation is to better understand how P. carotovorum transitions from an environmental microbe to a pathogen, and the role of the T3SS in that process. In the first chapter, I review how virulence factors, such as plant degrading enzymes and the T3SS, are regulated in P. carotovorum, and compare its regulation strategy to that of other plant pathogens. In the second chapter, I present an analysis, published with our collaborators, of the genome sequence of P. carotovorum, which we draw upon in the subsequent chapters. The third chapter evaluates transcriptional data during tuber, stem and leaf infections and suggests a tissue-specific role for the T3SS during infection. Lastly, the fourth chapter presents data that suggests carbon source availability is involved in tissue-specific virulence regulation. In conclusion, this dissertation furthers our understanding of the virulence strategy of P. carotovorum. |
