UC Davis

Plants’ innate immunity is composed of two intricate immune networks: pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is activated upon the recognition of pathogen-associated molecular patterns (PAMPs) by a pattern recognition receptor (PRRs). The outcomes of PTI are considered broad spectrum but can be easily suppressed by effectors from the adapted pathogens. Perception of the pathogen effectors by a nucleotide-binding leucine-rich (NLR) receptor activates ETI, which leads to a robust response in the form of localized programmed cell death at the site of infection. NLRs are classified into different classes based on protein structures: coiled-coil NLRs (CNLs) and Toll/interleukin-1 NLRs (TNLs). Both types deploy common and unique mechanisms to achieve immunity. CNLs can function as singletons, linked pairs or complex networks. Meanwhile, TNLs rely on the downstream immune modulator, ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1). EDS1 coordinates with RPW8-like NLRs (RNLs) to attain the defense response. In this dissertation, I describe the current knowledge and perspectives about the major types of NLRs in plants, including their discovery and functions, and various mechanisms they utilize to establish immunity. I also present findings of my studies, in which the regulation of EDS1 immune signaling is elucidated by TurboID-based proximity labeling proteomics. A unique NLR, belonging to the NLR-requirement for cell death (NRC) family, is identified as a negative regulator of TNL-mediated immunity. The connection between autophagy and TNL immune network is revealed in this work from the demonstration of interactions between autophagy-related gene 6 (ATG6) and the EDS1 complexes. Overall, this dissertation contributes to a better understanding of EDS1 immune signaling in plants and highlights the interplays amongst different classes of NLRs, and also autophagy as ways to fine-tune TNL-mediated immunity.