Utilizing natural and engineered viruses is an accepted approach to studying plant-virus interactions as it relates to symptomology. The majority of the research topics were generated by deciphering where short-comings in the literature existed. Specifically, how Turnip mosaic virus (TuMV) helper component protease (HC-Pro) small RNA (sRNA) binding affinity affects expression of genes correlated with disease phenotypes and studying debilitated viruses in a variety of RNA silencing deficient Arabidopsis thaliana plants. Taken as a whole, the research presented addressed the susceptibility of A. thaliana to TuMV.

The first study was conducted to monitor genes implicated in symptomology in various RNA silencing pathway mutant backgrounds. I hypothesized that an in vitro approach, in conjunction with an in silico study would reveal the mechanism TuMV utilizes to regulate sRNA expression, post-infection. The second study focused on severe, moderate, and weak TuMV strains, versus A. thaliana response to pathogen challenge. I hypothesized that TuMV HC-Pro FRNK box mutants that differed in their ability to infect plants affected the function of host sRNA in graduated steps. I also postulated that these mutants might allow me to uncouple developmental abnormalities associated with disease progression and accumulation of the virus itself. In the final study, I combined my passion for plant pathology and molecular techniques to explore a topic unrelated to potyviruses.

Conclusions based on analyzing the transcripts and sRNAs of genes correlated with TuMV disease symptomology, quantifying their expression in wild-type and RNA silencing defective A. thaliana plants, and characterizing various TuMV viruses lacking RNA silencing suppressor activity will be discussed. Future directions will also be introduced.