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The role of salicylic acid receptors NPR1 and NPR3/4 in PAMP-triggered immunity and effector-triggered immunity Radojicic, Ana

Abstract

Plants are constantly exposed to different pathogens in their environment and they have evolved complex defense strategies to avoid potential disease. The two general layers of plant defense are pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is activated upon recognition of PAMPs by plant’s pattern recognition receptors (PRRs) localized on plasma membrane, while ETI is triggered when the presence of bacterial effector proteins is detected by intracellular plant nucleotide-binding leucine-rich repeat (NLR) proteins. Salicylic acid (SA) is a major regulator of plant immunity. A new model of SA signaling in Arabidopsis thaliana was recently established. Non-expressor of Pathogenesis-Related (PR) genes 1 (NPR1), NPR3 and NPR4 are SA receptors that have opposite roles in transcriptional regulation of defense-related genes. NPR1 functions as a transcriptional co-activator, while NPR3 and NPR4 are redundant transcriptional co-repressors of defense-related genes. Binding of SA activates NPR1, while it blocks transcriptional repression activity of NPR3 and NPR4. Although general function of these proteins in plant defense is understood, their requirement for different regulatory pathways in plant immunity is not entirely explored. In this thesis I analyze how NPR1 and NPR3/4 are involved in regulation of PTI response, and ETI response mediated by different NLR proteins. Infection assays with different strains of Pseudomonas syringae pv. tomato DC3000 revealed that PTI is regulated through both NPR1- and NPR3/4-dependent signaling, and that basal levels of SA contribute to PTI and AvrRPS4- or AvrRpt2-triggered ETI. The knock-out mutant npr1-1 and a dominant gain-of-function mutant allele npr4-4D fully suppress expression of PR1 and resistance to H.a. Noco2, but partially suppress dwarf morphology and constitutive PR2 expression of autoimmune snc1 mutant. Similarly, npr1-8 and npr4-4D partially suppress autoimmune phenotype of mkk1/2 mutants. Results of ion-leakage assay suggest that SA serves as a negative regulator of AvrRpt2-triggered hypersensitive response through NPR1 and NPR4-mediated signaling. My results support the new model of SA-dependent signaling, confirming that NPR1 and NPR3/4 function in parallel pathways. Although SA is the major regulator of plant defense, not all aspects of immune response rely entirely on SA receptors NPR1 and NPR3/4, confirming existence of SA-independent signaling.

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