Signaling by small metabolites in systemic acquired resistance

Abstract

SUMMARYPlants can retain the memory of a prior encounter with a pest. This memory confers upon a plant the ability to subsequently activate defenses more robustly when challenged by a pest. In plants that have retained the memory of a prior, localized, foliar infection by a pathogen, the pathogen-free distal organs develop immunity against subsequent infections by a broad-spectrum of pathogens. The long-term immunity conferred by this mechanism, which is termed systemic acquired resistance (SAR), is inheritable over a few generations. Signaling mediated by the phenolic metabolite salicylic acid (SA) is critical for the manifestation of SAR. Recent studies have described the involvement of additional small metabolites in SAR signaling, including methyl salicylate, the abietane diterpenoid dehydroabietinal, the lysine catabolite pipecolic acid, a glycerol-3-phosphate-dependent factor and the dicarboxylic acid azelaic acid. Many of these metabolites can be systemically transported through the plant and probably facilitate communication by the primary infected tissue with the distal tissues, which is essential for the activation of SAR. Some of these metabolites have been implicated in the SAR-associated rapid activation of defenses in response to subsequent exposure to the pathogen, a mechanism termed priming. Here, we summarize the role of these signaling metabolites in SAR, and the relationship between them and SA signaling in SAR.

Comparative Proteomics Analysis of Arabidopsis Phloem Exudates Collected During the Induction of Systemic Acquired Resistance

“…The lipid transfer protein (LTP) DIR1 is currently the only protein demonstrated to move from SARinduced to distant tissues via the phloem (Champigny et al, 2013). Recent studies demonstrate that DIR1 interacts with other SAR-related LTPs in untreated tobacco leaves (Yu et al, 2013;Cecchini et al, 2015) and is associated with a dehydroabietinal-containing, trypsinsensitive, high-molecular-weight fraction of phloem exudates collected from SAR-induced leaves (Shah et al, 2014). This suggests that DIR1 is a member of a large proteinaceous complex that travels to distant leaves in the phloem during SAR.…”

The Roles of ROS and ABA in Systemic Acquired Acclimation

“…These include, among others, salicylic acid and methyl salicylate, jasmonic acid and methyl jasmonate, azelaic acid, auxin, ethylene, abscisic acid (ABA), reactive oxygen species (ROS), different peptides and proteins, electric signals, and RNA molecules (Karpi nski et al, 2013;Shah et al, 2014;Wang et al, 2014;Wendehenne et al, 2014). These chemicals and compounds were proposed to function alone or to interact with each other and to mediate or regulate systemic responses.…”

“…The presumed common outcome of all of these systemic responses is to alert all remote and unstressed tissues of the plant to the existence of a biotic or abiotic threat and to trigger the activation of resistance or acclimation pathways in these tissues. These responses typically are measured by enhanced accumulation of defense or acclimation transcripts and proteins and/or by demonstrating an enhanced level of tolerance or resistance to a subsequent abiotic or biotic stress applied to systemic tissues (Karpi nski et al, 2013;Suzuki et al, 2013;Gilroy et al, 2014;Shah et al, 2014). Activating resistance or acclimation pathways in remote tissues that were not yet subjected to the stress or pathogen would therefore enable the plant to withstand and survive the upcoming biotic or abiotic challenge.…”

Bacteria-Triggered Systemic Immunity in Barley Is Associated with WRKY and ETHYLENE RESPONSIVE FACTORs But Not with Salicylic Acid

“…These signals include the methylated derivative of SA methyl salicylate (Park et al, 2007), glycerol-3-phosphate (Chanda et al, 2011), the diterpenoid dehydroabietinal (Chaturvedi et al, 2012), the C 9 dicarboxylic acid azelaic acid (Jung et al, 2009), and the lipid transfer proteins DEFECTIVE IN INDUCED RESISTANCE1 (DIR1; Maldonado et al, 2002), DIR1-like (Champigny et al, 2013), and AZELAIC ACID INDUCED1 (AZI1; Jung et al, 2009). Glycerol-3-phosphate might be part of a positive feedback loop, with DIR1 and AZI1 acting downstream of azelaic acid (Yu et al, 2013;Gao et al, 2014;Shah et al, 2014), which accumulates by autooxidation of C18 unsaturated fatty acids, possibly downstream of nitric oxide and reactive oxygen species, to promote SAR (Zoeller et al, 2012;Wang et al, 2014;Wittek et al, 2014). In addition, the nonprotein amino acid pipecolic acid is essential for SAR (Návarová et al, 2012;Shah and Zeier, 2013;Zeier, 2013).…”