정의환 연구실

Plants defend against pathogen infection by both passive and active immune mechanisms. During co-evolution, pathogens that confront the plant’s defenses modify host signaling components for successful colonization. Plants can subsequently monitor pathogen-driven changes and activate additional immune responses. The plant innate immunity consists of two tiers for governing the recognition of pathogens. The first layer is mediated by cell-surface receptors that perceive evolutionarily conserved pathogen (or microbe)-associated molecular patterns (PAMPs/MAMPs). These are typically LRR-kinases and LysM-kinases that can turn on immune responses, lead to transcriptional re-programing, and generate anti-microbial compounds. This immune response is PAMPs (MAMPs)-triggered immunity or PTI (MTI). Pathogens have evolved mechanisms that overcome PTI and induce disease in host plants. They deploy a series of virulence factors known as effector proteins to dampen the PTI response by targeting host proteins participating in key immune signaling pathways. To monitor the mode of function or structure of pathogen effector proteins and activate efficient defense responses in host cells, plants have evolved nucleotide binding leucine-rich repeat (NLR) proteins that initiate the second layer of immunity, effector-triggered immunity or ETI. The current and long-term research objective in PIPL is to (i) provide a mechanistic understanding of the function of pathogen-secreted effector proteins that suppress the plant immune response and (ii) determine unique and common mechanisms that exclude pathogens through the deployment of both PTI (MTI) and ETI responses in plants. This research program is expected to contribute to dissection of the complex relationships that exist between host and their