Grant: Discovery Grants Program - Individual

Plant diseases account for 15% of annual global crop losses (estimated worth of $100 billion) and currently require costly and environmentally unfriendly chemical treatments. Pathogens are capable of infecting crops and causing disease largely because they can suppress plant immune responses. Thus, only when we clearly understand the plant immune system will we be able to offer safe and sustainable solutions to diseases that affect our crops. Because pathogen responses necessarily re-direct plant energy away from growth, a major challenge is how to boost plant immunity without affecting yield.The long-term goal of my research program is to understand the molecular mechanisms that tailor plant immune signaling to maintain cellular homeostasis in the model plant Arabidopsis thaliana. I am particularly interested in how immune signaling enzymes are regulated by post-translational modifications and differential binding partners/substrates, and how positive and negative signaling cascades are established and controlled. The proposed research addresses the impact of immune signaling on plant homeostasis at the molecular level and integrates molecular and cell biology, biochemistry, and proteomics with forward- and reverse-genetics. Owing to the multi-disciplinary nature of our research program, lab personnel will be trained in a broad range of techniques spanning molecular biology, biochemistry, and plant genetics.Arabidopsis and other plants perceive pathogens via receptor kinases located at the cell surface. The kinase BIK1 is phosphorylated (and activated) by several receptors and is integral to plant immune signaling. Demonstrating its importance, BIK1 is the target of multiple unrelated pathogens to dampen immune signaling. We recently showed that plants maintain an optimal level of BIK1 through a process of continuous proteasomal degradation influenced by the kinase CPK28, which also interacts with and phosphorylates BIK1. Thus, it seems that BIK1 is both positively and negatively regulated by phosphorylation, raising the intriguing possibility that residue-specific or quantitative differences contribute to the two states. We will characterize phosphorylation and subsequent ubiquitination events on BIK1 and study how these events control its turnover. Furthermore, we will identify the E3 ligase(s) responsible for BIK1 degradation. To understand more about how CPK28 is regulated, will characterize CPK28-associated proteins that we recently identified by mass-spectrometry. Because of the need to identify novel proteins involved in plant immune signaling that may also be pathogen targets, we will also screen for such proteins using forward-genetics. My program provides an excellent training environment for HQP to make a high impact in plant molecular biology using state-of-the-art technologies that will inform agricultural practices in Canada and world-wide.