Abstract

Salicylic acid (SA) is a phytohormone that plays important roles in many aspects of plant life, notably in plant defenses against pathogens. Key mechanisms of SA signal transduction pathways have now been uncovered. Even though details are still missing, we understand how SA production is regulated and which molecular machinery is implicated in the control of downstream transcriptional responses. The NPR1 pathway has been described to play the main role in SA transduction. However, the mode of SA perception is unclear. NPR1 protein has been shown to bind SA. Nevertheless, NPR1 action requires upstream regulatory events (such as a change in cell redox status). Besides, a number of SA-induced responses are independent from NPR1. This shows that there is more than one way for plants to perceive SA. Indeed, multiple SA-binding proteins of contrasting structures and functions have now been identified. Yet, all of these proteins can be considered as candidate SA receptors and might have a role in multinodal (decentralized) SA input. This phenomenon is unprecedented for other plant hormones and is a point of discussion of this review.

Highlights

  • Salicylic acid (SA, 2-hydroxybenzoic acid) is a phenolic plant hormone

  • Monomeric Nonexpressor of Pathogenesis-related protein 1 (NPR1) shuttles to nuclei where it interacts with TGA transcription factors leading to the expression of PATHOGENESIS-RELATED (PR) genes involved in the set-up of plant immune defenses [13]

  • In A. thaliana, 18 SABP2 orthologues were identified and at least five proteins (AtMES1,2,4,7,and -9) were shown to possess an esterase activity acting on methyl salicylate (MeSA) that was inhibited by SA in vitro [66]

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Summary

Introduction

Salicylic acid (SA, 2-hydroxybenzoic acid) is a phenolic plant hormone. SA has a well- documented role in plant responses to environmental stresses including chilling [1], freezing [2,3], heat [4], heavy metals [5], salt [6], drought [7] and, notably, reactions to biotrophic pathogens [8]. Pseudomonas Susceptibility 1; GH3.5, Gretchen Hagen 3.5; ICS, isochorismate synthase; IC-Glu, Susceptibility 1; GH3.5, Gretchen Hagen 3.5; ICS, isochorismate synthase; IC-Glu, isochorismate-9-glutamate; IPL, isochorismate pyruvate lyase; MeSA, methyl-salicylate; MES, isochorismate-9-glutamate; IPL, isochorismate pyruvate lyase; MeSA, methyl-salicylate; MES, methyl-salicylate esterase; MT, metyl transferase; PAL, phenylalanine ammonia-lyase; PBS3, avrPphB methyl-salicylate esterase; MT, metyl transferase; PAL, phenylalanine ammonia-lyase; PBS3, susceptible 3; SAG, salicylic acid glucoside; SAH, salicylic acid hydroxylase; SGE, salicylic avrPphB susceptible 3; SAG, salicylic acid glucoside; SAH, salicylic acid hydroxylase; SGE, salicylic acid glucose ester; SOT12, sulfotransferase 12; UDP-GST, UDP-glycosyltransferase; UGT76D1, acid glucose ester; SOT12, sulfotransferase 12; UDP-GST, UDP-glycosyltransferase; UGT76D1, UDP-glycosyltransferase 76D1; *, enzyme not cloned in plants; **, non-enzymatic decay Another pathway for SA synthesis involves the phenylalanine ammonia lyase (PAL) converting phenylalanine (Phe) to trans-cinnamic acid. Monomeric NPR1 shuttles to nuclei where it interacts with TGA transcription factors leading to the expression of PATHOGENESIS-RELATED (PR) genes involved in the set-up of plant immune defenses [13]. The role(s) of such a multitude of SABPs is still unexplained and offers a new paradigm for hormonal regulation in plants

SA Binding Proteins
SABP1—Catalase
SABP2—MeSA Esterase
SABP3—β Carbonic Anhydrase
Thioredoxins
GH3—Acyl Acid Amido Synthetase
Alpha-ketoglutarate Dehydrogenase—Krebs Cycle Enzyme
2.11. MORC Proteins—Epigenetic Regulation
2.12. HMGB3—DAMP Protein
Molecular Mechanisms of SA-Protein Interactions
Schematic
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