Abstract

The master regulator of salicylic acid (SA)-mediated plant defense, NPR1 (NONEXPRESSER OF PR GENES 1) and its paralogs NPR3 and NPR4, act as SA receptors. After the perception of a pathogen, plant cells produce SA in the chloroplast. In the presence of SA, NPR1 protein is reduced from oligomers to monomers, and translocated into the nucleus. There, NPR1 binds to TGA, TCP, and WRKY transcription factors to induce expression of plant defense genes. A list of compounds structurally similar to SA was generated using ChemMine Tools and its Clustering Toolbox. Several of these analogs can induce SA-mediated defense and inhibit growth of Pseudomonas syringae in Arabidopsis. These analogs, when sprayed on Arabidopsis, can induce the accumulation of the master regulator of plant defense NPR1. In a yeast two-hybrid system, these analogs can strengthen the interactions among NPR proteins. We demonstrated that these analogs can induce the expression of the defense marker gene PR1. Furthermore, we hypothesized that these SA analogs could be potent tools against the citrus greening pathogen Candidatus liberibacter spp. In fact, our results suggest that the SA analogs we tested using Arabidopsis may also be effective for inducing a defense response in citrus. Several SA analogs consistently strengthened the interactions between citrus NPR1 and NPR3 proteins in a yeast two-hybrid system. In future assays, we plan to test whether these analogs avoid degradation by SA hydroxylases from plant pathogens. In future assays, we plan to test whether these analogs avoid degradation by SA hydroxylases from plant pathogens.

Highlights

  • Plant immunity can be described as consisting of four phases, known as the zig-zag model [1]

  • We demonstrate that a similar group of salicylic acid (SA) analogs that are functional in Arabidopsis are capable of strengthening the interactions between NPR1 and NPR3 homologs in Citrus sinensis

  • We found acetylsalicylate, 5-methylsalicylic acid, 5-fluoro-2-hydroxybenzoic acid, and 5-iodosalicylic acid to be reliable inducers of plant defense

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Summary

Introduction

Plant immunity can be described as consisting of four phases, known as the zig-zag model [1]. Pathogen-associated molecular pattern recognition results in PAMP-triggered immunity (PTI). PAMP-triggered immunity consists of an increase in cytosolic Ca2+ [5], oxidative burst [6], MAPK activation [7], ethylene production [8], stomatal closure, transcriptional reprogramming, accumulation of the plant defense hormone salicylic acid (SA) [9], and callose deposition [10]. This response is basal disease resistance against pathogens that can halt colonization. The loss of recognized effectors or the gain of novel effectors, causes selective pressure on the host to evolve new R proteins, resulting in ETI [1]

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