Abstract
Systemic acquired resistance (SAR) is an inducible defense mechanism in plants that confers enhanced resistance against a variety of pathogens. SAR is activated in the uninfected systemic (distal) organs in response to a prior (primary) infection elsewhere in the plant. SAR is associated with the activation of salicylic acid (SA) signaling and the priming of defense responses for robust activation in response to subsequent infections. The activation of SAR requires communication by the primary infected tissues with the distal organs. The vasculature functions as a conduit for the translocation of factors that facilitate long-distance intra-plant communication. In recent years, several metabolites putatively involved in long-distance signaling have been identified. These include the methyl ester of SA (MeSA), the abietane diterpenoid dehydroabietinal (DA), the dicarboxylic acid azelaic acid (AzA), and a glycerol-3-phosphate (G3P)-dependent factor. Long-distance signaling by some of these metabolites also requires the lipid-transfer protein DIR1 (DEFECTIVE IN INDUCED RESISTANCE 1). The relative contribution of these factors in long-distance signaling is likely influenced by environmental conditions, for example light. In the systemic leaves, the AGD2-LIKE DEFENSE RESPONSE PROTEIN1 (ALD1)-dependent production of the lysine catabolite pipecolic acid (Pip), FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1) signaling, as well as SA synthesis and downstream signaling are required for the activation of SAR. This review summarizes the involvement and interaction between long-distance SAR signals and details the recently discovered role of Pip in defense amplification and priming that allows plants to acquire immunity at the systemic level. Recent advances in SA signaling and perception are also highlighted.
Highlights
Plants employ multiple layers of defense to combat pathogens
In the pathogen-inoculated tissues, recognition by the plant of molecular patterns that are conserved amongst groups of microbes results in the activation of PTI (PAMP-triggered immunity), which contributes to basal resistance that controls the extent of pathogen growth
A G3P-dependent factor is likely involved in long-distance signaling. These results suggest that the systemic increase in G3P observed in systemic acquired resistance (SAR) likely results from de novo synthesis
Summary
Plants employ multiple layers of defense to combat pathogens. These defenses include a combination of preformed and inducible mechanisms (Jones and Dangl, 2006; Spoel and Dong, 2012). In the pathogen-inoculated tissues, recognition by the plant of molecular patterns that are conserved amongst groups of microbes results in the activation of PTI (PAMP-triggered immunity), which contributes to basal resistance that controls the extent of pathogen growth. SAR and ISR engage different mechanisms and as a result have an additive effect on foliar disease resistance (van Wees et al, 2000). SAR results in a heightened state of preparedness in the uninfected organs against subsequent infections. These tissues are primed to turn on defenses faster and stronger when challenged by pathogen (Conrath, 2011). Long-distance communication by the primary pathogen-infected organ with rest of the pathogen-free foliage is critical for the activation of SAR. In a series of grafting studies, they showed that the SAR signal can be transmitted from the pathogen-inoculated rootstock to the pathogen-free graft (scion)
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