The overall goal of this project is to understand mechanisms by which bacterial pathogens adapt to a plant host environment, an adaptation that is essential for bacterial survival and virulence. Knowing such mechanisms is required for efforts to control disease progression. When a bacterial plant pathogen infects a host, a tug-of-war ensues in which the plant host aims to defend itself against the pathogen; the bacterium in turn responds, often subverting host defenses by utilizing host-derived signals to trigger expression of traits that promote survival and virulence. This project focuses on mechanisms by which bacteria detect and respond to such host-derived signals. In addition, the program integrates research and teaching by offering the opportunity for both graduate and undergraduate students to acquire research experience and proficiency in modern molecular biology techniques. Graduate students will be integral to developing these research projects and in disseminating results. For undergraduate students, many of whom will be recruited from programs that promote inclusion and diversity, the opportunities for independent research will complement their regular course curriculum, prepare them for advanced studies, and contribute to the development of a competitive STEM workforce.
Hosts produce reactive oxygen species as a defense against a bacterial infection. One of the enzymes responsible for this oxidative burst is xanthine dehydrogenase, which converts hypoxanthine to xanthine and xanthine to urate. The first objective of this project is to address the hypothesis that the xanthine and urate that are produced by host plants during a bacterial infection function as diffusible signals to induce differential gene expression in the bacterium. The second goal is to investigate the role of the transcription factor PecS in sensing xanthine and urate and controlling gene expression. A combination of RNA-seq and ChIP-seq will be implemented to identify the PecS regulon, and phenotypes of pecS mutant strains predicted from RNA-seq data will be determined. Focusing on the plant pathogen Agrobacterium fabrum, the virulence of wild-type and pecS deletion mutant strains will be compared. Defining host-derived signals and the mechanisms by which these diffusible messengers trigger expression of virulence-associated genes in plant pathogens will ultimately facilitate development of antibacterial agents.
