UC Davis

As the world’s population grows, we must seek to enhance food production. One hurdle in the way of achieving this goal is the devastating loss caused by plant pathogens and pests. Plants are not completely defenseless against pathogenic attack and utilize a multilayered immune system to prevent disease. Recognition of pathogens involves dynamic signaling that activates multiple outputs with the overall goal of resistance. One of these outputs is the generation of reactive oxygen species (ROS) during pathogen recognition. In plants, production of ROS during infection is mediated by membrane localized NADPH oxidases which are more commonly known as respiratory burst oxidase homologs (RBOHs). Our understanding of activation of RBOHs is derived from research on RBOHD from Arabidopsis thaliana. However, our knowledge of how RBOHs are negatively regulated has been limited. In this dissertation, I studied a pathway that negatively regulates stability of RBOH and ROS production in Arabidopsis (Arabidopsis thaliana) and Tomato (Solanum lycopersicum). My results show that RBOHD is negatively regulated through crosstalk between phosphorylation and ubiquitination, which involves PIRE, an E3 ubiquitin ligase. Further analysis revealed that PIRE is conserved in land plants as are the phosphorylation signaling residues in RBOH homologs. Finally, utilizing gene editing tools, I show that this conserved pathway can be exploited to enhance production of ROS and disease resistance in tomato. Collectively, this dissertation work details the characterization of a novel regulatory pathway for RBOHD in A. thaliana and highlights the potential to utilize this knowledge as a foundation for translational work in tomato with the goal of enhancing resistant to pathogens.