Understanding local and systemic signaling pathways in plant immunity

点击翻译按钮获取中文摘要

Plants possess disease resistance pathways to combat microbial infections. Each year an estimated 10 to 40% of world food production is lost to disease despite resistant crop varieties and pesticide application. In view of these losses, the goal of my research is to understand plant immune responses to inform efforts to manipulate plant immunity to improve disease resistance in crops. In locally infected leaves, individual plant cells perceive pathogen-associated molecules called PAMPs to initiate PAMP-Triggered Immunity (PTI). Local defense can induce Systemic Acquired Resistance (SAR), in which mobile signals are produced and transported from induced to distant leaves to establish resistance to future pathogen attack. Some plants become more resistant to a particular pathogen as they age and exhibit Age-Related Resistance (ARR). For example, young 3 to 4 week-old Arabidopsis plants are susceptible to the bacterial pathogen, Pseudomonas syringae pathovar (pv) tomato (P.syringae), but exhibit resistance to the same pathogen as mature 6 to 7 week-old plants. My research team seeks to understand the molecular genetic and biochemical basis of plant immunity using the model system, Arabidopsis and P. syringae. We demonstrated that the plant hormone salicylic acid (SA) performs a previously unknown function as an antimicrobial agent that suppresses the growth and biofilm formation of P.syringae in plant intercellular spaces during ARR and PTI. Biofilms consist of adherent bacterial cells surrounded by an extracellular matrix that are thought to protect bacteria from host defense. To our knowledge, we are the first lab to show that P. syringae forms biofilms in leaf intercellular spaces and demonstrate that biofilm formation contributes to P.syringae success. We will perform parallel transcriptomic analysis of the plant and pathogen to understand how mature plants perceive normally virulent pathogens and how PTI- and ARR-responding plants inhibit P.syringae biofilm formation. My lab has made significant progress in understanding how SAR mobile signals including DIR1 access the phloem for movement from induced to distant leaves and identified proteins that accumulate in the phloem and contribute to SAR, perhaps by interacting with DIR1. We will take advantage of DIR1's role in both SAR-induced and distant leaves to identify the molecular components responsible for DIR1 movement out of SAR-induced leaves and identify DIR1 interactors that restrict its movement under non-inductive conditions and/or facilitate DIR1 movement upon SAR activation by performing DIR1 movement assays using SAR mutants and protein-protein assays (TurboID, co-IPs + LC-MS/MS). DIR1's cellular route during SAR will also be examined by conditionally blocking access to the phloem to observe the effect on movement of DIR1-iLOV (iLOV:fluorescent peptide), monitored using fluorescence microscopy, to reveal fundamental cellular information about the path taken by DIR1 during SAR.