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Abstract
To combat bacterial disease, we must first understand the mechanics of infection. Biologists can study plant pathogens as model organisms to elucidate the processes that all disease-causing bacteria use to establish effective infections. The bacterium Agrobacterium tumefaciens infects plants to cause crown gall disease, which can substantially reduce the yield of many important food crops. In order for A. tumefaciens cells to infect plants, the bacteria must swim through the soil towards susceptible plant hosts and successfully attach to plant surfaces. This dissertation focuses on the mechanisms by which A. tumefaciens cells sense plant signals and integrate those signals to modulate their swimming and attachment capabilities. My research shows that at least two global regulatory pathways control swimming and attachment. In this doctoral work, I describe how one pathway functions to activate swimming motility and attachment, while the other pathway acts to suppress swimming motility and surface attachment mechanisms in response to low pH, a condition that is encountered during host interactions. The first of these control pathway transcriptionally controls motility-related functions, while the second, pH-responsive pathway is much broader, and controls a large number of genes of which the motility functions are a subset. In this work, I discuss several models for how these two pathways interact with each other to direct important cellular processes and report how I tested these models. The discovery of the convergence points of these two regulatory networks is also described. This work furthers our understanding about how pathogenic bacteria acclimate to potential hosts and use signals from this environment to regulate infection processes. The infection processes discussed here are so early in an infection cycle that knowledge of their regulation may be informative in preventing the establishment of bacterial infections.
