Plastid ω3‐fatty acid desaturase‐dependent accumulation of a systemic acquired resistance inducing activity in petiole exudates of Arabidopsis thaliana is independent of jasmonic acid

Abstract

SummarySystemic acquired resistance (SAR) is an inducible defense mechanism that is activated throughout the plant, subsequent to localized inoculation with a pathogen. The establishment of SAR requires translocation of an unknown signal from the pathogen-inoculated leaf to the distal organs, where salicylic acid-dependent defenses are activated. We demonstrate here that petiole exudates (PeXs) collected from Arabidopsis leaves inoculated with an avirulent (Avr) Pseudomonas syringae strain promote resistance when applied to Arabidopsis, tomato (Lycopersicum esculentum) and wheat (Triticum aestivum). Arabidopsis FATTY ACID DESATURASE7 (FAD7), SUPPRESSOR OF FATTY ACID DESATURASE DEFICIENCY1 (SFD1) and SFD2 genes are required for accumulation of the SAR-inducing activity. In contrast to Avr PeX from wild-type plants, Avr PeXs from fad7, sfd1 and sfd2 mutants were unable to activate SAR when applied to wild-type plants. However, the SAR-inducing activity was reconstituted by mixing Avr PeXs collected from fad7 and sfd1 with Avr PeX from the SAR-deficient dir1 mutant. Since FAD7, SFD1 and SFD2 are involved in plastid glycerolipid biosynthesis and SAR is also compromised in the Arabidopsis monogalactosyldiacylglycerol synthase1 mutant we suggest that a plastid glycerolipid-dependent factor is required in Avr PeX along with the DIR1-encoded lipid transfer protein for long-distance signaling in SAR. FAD7-synthesized lipids provide fatty acids for synthesis of jasmonic acid (JA). However, co-infiltration of JA and methylJA with Avr PeX from fad7 and sfd1 did not reconstitute the SAR-inducing activity. In addition, JA did not co-purify with the SAR-inducing activity confirming that JA is not the mobile signal in SAR.

Loss of Function of FATTY ACID DESATURASE7 in Tomato Enhances Basal Aphid Resistance in a Salicylate-Dependent Manner

“…Further work is needed to explore the potential interaction between NPR1 on fatty acid metabolism. Additional studies are also necessary to determine if aphid resistance in Arabidopsis FAD mutants is also SA dependent, particularly in light of recent conflicting reports about the potential impacts of FAD7 on SA signaling in this species (Chaturvedi et al, 2008;Xia et al, 2010). However, our findings are consistent with other studies indicating that SA can contribute to plant defenses against aphids in other tomato genotypes.…”

Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis

“…Moreover, DEFECTIVE IN INDUCED RESISTANCE1 (DIR1) bears homology to lipid transfer proteins and is involved in local generation or subsequent translocation of a mobile systemic signal, possibly by acting as a chaperone for a lipid-related signal (Maldonado et al, 2002). A glycerolipid-derivative might be a DIR1-interacting partner because the dihydroxyacetone phosphate reductase SUPPRES-SOR OF FATTY ACID DESATURASE ACTIVITY1 (Nandi et al, 2004) and the fatty acid desaturase FAD7, both components of plastid glycerolipid biosynthesis, are necessary for SAR establishment and, together with DIR1, are required for the accumulation of a SAR-inducing activity in Arabidopsis petiole exudates (Chaturvedi et al, 2008). Moreover, the plant defense hormone jasmonic acid (JA) or a JA pathway-related oxylipin was proposed as the signal mediating long-distance information transmission during SAR (Truman et al, 2007).…”

“…Mutational analyses in Arabidopsis suggest that peptide and lipid derivatives participate in signal transduction from inoculated to distant leaves (Grant and Lamb, 2006;Chaturvedi et al, 2008). A peptide signal might be generated by the apoplastic aspartic protease CONSTITUTIVE DISEASE RESISTANCE1, which is required for the execution of both local and systemic resistance responses (Xia et al, 2004).…”

Next-Generation Systemic Acquired Resistance

“…The exact nature of the systemic SAR signal in Arabidopsis (Arabidopsis thaliana) after localized infection by avirulent Pseudomonas syringae remains complex and has been a matter of debate (Attaran et al, 2009). Apart from methyl salicylate (MeSA; Vlot et al, 2008aVlot et al, , 2008b, glycerolipids (Chaturvedi et al, 2008), azeleic acid (Jung et al, 2009), and glycerol-3-P (Chanda et al, 2011) have been implicated. As a plausible explanation, Liu et al (2011b) recently proposed that SAR is controlled by an interaction between at least two mobile signals, MeSA and a complex formed between the lipid transfer protein DIR1 and glycerolipid or lipid derivatives.…”