Activation Of Systemic Acquired Resistance Research Articles

RSI1/FLD and its epigenetic target RRTF1 are essential for the retention of infection memory in Arabidopsis thaliana.

Plants can retain a memory of previous pathogen infections to mount a more robust defense response during subsequent infections by developing systemic acquired resistance (SAR). However, the mechanism through which plants develop and retain infection memory is not known. Experiments have shown the association of epigenetic modifications of specific defense-related genes with SAR. RSI1/FLD codes for a histone demethylase and is required for the activation of SAR in Arabidopsis. Here we report the identification of RRTF1 as an epigenetic target of RSI1. RRTF1 expression is higher in pathogen-free distal tissues of the rsi1 mutant. Experiments with loss-of-function and overexpression lines suggest RRTF1 is a negative regulator of basal defense against virulent and avirulent pathogens as well as SAR. Enhanced expression of RRTF1 in a wild-type (WT) background specifically impairs SAR without impacting local resistance. RSI1 is recruited at the RRTF1 locus in a SAR-inducible manner and contributes to H3K4me2 and H3K4me3 demethylation. Introduction of the rrtf1 mutation rescues the loss-of-SAR phenotype of rsi1 plants. However, these plants fail to retain infection memory beyond 7 days post-primary inoculation, whereas WT plants retain memory for at least 11 days. Our results demonstrate that RSI1 and RRTF1 form a functional module for retaining infection memory in Arabidopsis.

Pipecolic acid synthesis is required for systemic acquired resistance and plant-to-plant-induced immunity in barley.

Defense responses in plants are based on complex biochemical processes. Systemic acquired resistance (SAR) helps to fight infections by (hemi-)biotrophic pathogens. One important signaling molecule in SAR is pipecolic acid (Pip), accumulation of which is dependent on the aminotransferase ALD1 in Arabidopsis. While exogenous Pip primes defense responses in the monocotyledonous cereal crop barley (Hordeum vulgare), it is currently unclear if endogenous Pip plays a role in disease resistance in monocots. Here, we generated barley ald1 mutants using CRISPR/Cas9, and assessed their capacity to mount SAR. Endogenous Pip levels were reduced after infection of the ald1 mutant, and this altered systemic defense against the fungus Blumeria graminis f. sp. hordei. Furthermore, Hvald1 plants did not emit nonanal, one of the key volatile compounds that are normally emitted by barley plants after the activation of SAR. This resulted in the inability of neighboring plants to perceive and/or respond to airborne cues and prepare for an upcoming infection, although HvALD1 was not required in the receiver plants to mediate the response. Our results highlight the crucial role of endogenous HvALD1 and Pip for SAR, and associate Pip, in particular together with nonanal, with plant-to-plant defense propagation in the monocot crop barley.

Management of Chilli anthracnose/die-back or fruit rot by systemic acquired resistance activators

Chilli is an important spice, vegetable as well as cash crop of Gujarat, mostly cultivated in Kharif season, which is quite remunerative to farmers. Chilli is prone to several diseases, but anthracnose is a most devastating caused by fungus Colletotrichum capsici (Sydow) Butler and Bisby and one of the major constraints in chilli cultivation throughout the world. In the present study various systemic acquired resistance activators tested against chilli anthracnose during 2018, 2019 and 2020 at College of Horiculture, S.D. Agricultural University, Jagudan, Mehsana Gujarat. Data clearly revealed that minimum per cent disease intensity and highest green chilli yield was observed in seed soaking + foliar spray of Azoxystrobin 1000 ppm which was at par with seed soaking + foliar spray of Salicylic acid (SA) 100 ppm during individual year and pooled data also. Azoxystrobin and Salicylic acid (SA) induced systemic acquired resistance by increasing defense enzymes peroxidase (PO), polyphenol oxidase (PPO), phenylalanine ammonia lyase (PAL), -1, 3 glucanase, chitinase, catalase and defense-inducing chemicals (total phenols). Azoxystrobin is also registered in CIBRC for management of chilli anthracnose with PHI 5 days

Management of Chilli anthracnose/die-back or fruit rot by systemic acquired resistance activators

Management of Chilli anthracnose/die-back or fruit rot by systemic acquired resistance activators

POWERDRESSpositively regulates systemic acquired resistance in Arabidopsis.

PWR, an epigenetic regulator, and PIF4, a transcription factor coordinately regulate both local resistance and systemic acquired resistance in Arabidopsis. A plant that gets infected once becomes resistant to subsequent infections through the development of systemic acquired resistance (SAR). Primary-infected tissues generate mobile signals that travel to systemic tissues and cause epigenetic changes associated with the SAR activation. Epigenetic regulators and the process of infection memory development are largely obscure for plants. POWERDRESS (PWR), a SANT domain-containing histone deacetylation (HDAC) promoting gene, is essential for thermomorphogenesis. Here we show that PWR is required for the SAR activation in Arabidopsis. The pwr mutants in Ler and Col-0 background possess normal local resistance but are defective in SAR. PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) genetically interacts with PWR for flowering and thermomorphogenesis and is a negative regulator of basal immunity. We found a cooperative function for suppressing basal immunity and SAR activation by PIF4 and PWR, respectively. PWR promotes the expression of SA biosynthesis genes and the accumulation of SA in the systemic tissues. RSI1/FLD, which influences histone methylation and acetylation, is essential to infection memory development in Arabidopsis. Our results show that PWR and RSI1 positively regulate each other's expression. Exogenous application of HDAC inhibitor sodium butyrate abolishes SAR-mediated SA accumulation, expression of PR1 gene, and protection against pathogens after challenge inoculation. The results indicate the possibility of the involvement of HDAC activity of PWR in the formation of infection memory development in Arabidopsis.

'Candidatus Liberibacter asiaticus'-Encoded BCP Peroxiredoxin Suppresses Lipopolysaccharide-Mediated Defense Signaling and Nitrosative Stress In Planta.

The lipopolysaccharides (LPS) of gram-negative bacteria trigger a nitrosative and oxidative burst in both animals and plants during pathogen invasion. Liberibacter crescens strain BT-1 is a surrogate for functional genomic studies of the uncultured pathogenic 'Candidatus Liberibacter' spp. that are associated with severe diseases such as citrus greening and potato zebra chip. Structural determination of L. crescens LPS revealed the presence of a very long chain fatty acid modification. L. crescens LPS pretreatment suppressed growth of Xanthomonas perforans on nonhost tobacco (Nicotiana benthamiana) and X. citri subsp. citri on host orange (Citrus sinensis), confirming bioactivity of L. crescens LPS in activation of systemic acquired resistance (SAR). L. crescens LPS elicited a rapid burst of nitric oxide (NO) in suspension cultured tobacco cells. Pharmacological inhibitor assays confirmed that arginine-utilizing NO synthase (NOS) activity was the primary source of NO generation elicited by L. crescens LPS. LPS treatment also resulted in biological markers of NO-mediated SAR activation, including an increase in the glutathione pool, callose deposition, and activation of the salicylic acid and azelaic acid (AzA) signaling networks. Transient expression of 'Ca. L. asiaticus' bacterioferritin comigratory protein (BCP) peroxiredoxin in tobacco compromised AzA signaling, a prerequisite for LPS-triggered SAR. Western blot analyses revealed that 'Ca. L. asiaticus' BCP peroxiredoxin prevented peroxynitrite-mediated tyrosine nitration in tobacco. 'Ca. L. asiaticus' BCP peroxiredoxin (i) attenuates NO-mediated SAR signaling and (ii) scavenges peroxynitrite radicals, which would facilitate repetitive cycles of 'Ca. L. asiaticus' acquisition and transmission by fecund psyllids throughout the limited flush period in citrus.[Formula: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Reduced Infestation by Xylosandrus germanus (Coleoptera: Curculionidae: Scolytinae) in Apple Trees Treated with Host Plant Defense Compounds.

The ambrosia beetle Xylosandrus germanus (Blandford) is an invasive pest that has caused tree decline and death in numerous NY dwarf apple orchards during the past ten years, despite efforts to control them using trunk sprays of chlorpyrifos or pyrethroids, either alone or combined with the repellent verbenone. From 2017 to 2019, we tested trunk applications of different repellents and plant defense compounds for protection against X. germanus in potted apple trees adjacent to infested orchards. Treatments included topical formulations of verbenone and methyl salicylate (MeSa), alone and in combination, at different rates and timings. Additional treatments evaluated included the systemic acquired resistance activators acibenzolar-S-methyl, Reynoutria sachalinensis extract, and salicylic acid. The combination verbenone+MeSa treatments had the lowest incidences of attack sites and galleries containing adults or brood, although results varied among years. In a separate trial, we found no significant difference in numbers of adults caught in ethanol-baited traps placed 5-20 m from an apple bolt treated with the verbenone+MeSa repellent, suggesting that the repellent's effect did not extend to those distances from the treated target. Cross-sectional discs of trunk tissue sampled in August were analyzed for levels of phytohormones. Quantities of ergosterol, abscissic acid, salicylic acid, jasmonic acid, methyl salicylate, methyl jasmonate, trans-cinnamic acid, and indole-3-cinnamic acid did not significantly vary across treatments; however, trees with greater beetle damage contained higher levels of jasmonic and salicylic acid, which are key molecules in plant defense pathways.

Recombinant Protein Foliar Application Activates Systemic Acquired Resistance and Increases Tolerance against Papaya Dieback Disease

Similar to animals, plants possess ‘immune memory’ in response to invading pathogens that lead to enhanced defense reaction following pathogen exposure. Systemic acquired resistance (SAR) is a well-characterized type of plant immunity and is associated with coordinated expression of a set of pathogenesis-related (PR) genes and proteins also known as SAR markers. Induction of SAR in plants was shown to be initiated by group of chemicals and biological compounds known as SAR inducers that can be used for the management of important plant diseases. Elucidation and characterization of potential SAR inducers as potential elicitors that can protect papaya from the papaya dieback disease pathogen were carried out using HRPX protein, which was produced as a recombinant protein in an Escherichia coli system. Disease severity analysis in a glasshouse experiment indicated lower disease infection rates in the HRPX-treated plants than in water-treated plants. Selected SAR-associated defense gene expression was also shown to increase in treated plants, via quantitative real-time PCR analysis, confirming enhanced disease response through SAR activation. In this report, the selected recombinant protein was shown to activate the SAR mechanism in papaya for increased tolerance against papaya dieback disease, which was proven via physiological and molecular analysis.

Nitrogen-doped carbon dots alleviate the damage from tomato bacterial wilt syndrome: systemic acquired resistance activation and reactive oxygen species scavenging

Nitrogen doped carbon dots suppressed bacterial wilt in tomato through photosynthesis modulation, ROS scavenging, and resistance activation.

Systemicacquired resistance specific proteome of Arabidopsis thaliana.

A comparative proteomic study between WT and SAR-compromised rsi1/fld mutant reveals a set of proteins having possible roles in the SAR development. A partly infected plant shows enhanced resistance during subsequent infection through the development of systemic acquired resistance (SAR). Mobile signals generated at the site of primary infection travel across the plant for the activation of SAR. These mobile signals are likely to cause changes in the expression of a set of proteins in the distal tissue, which contributes to the SAR development. However, SAR-specific proteome is not revealed for any plant. The reduced systemic immunity 1 (rsi1)/(allelic to flowering locus D; fld) mutant of Arabidopsis is compromised for SAR but shows normal local resistance. Here we report the SAR-specific proteome of Arabidopsis by comparing differentially abundant proteins (DAPs) between WT and fld mutant. Plants were either mock-treated or SAR-induced by primary pathogen inoculation. For proteomic analysis, samples were collected from the systemic tissues before and after the secondary inoculation. Protein identification was carried out by using two-dimensional gel electrophoresis (2-DE) followed by tandem mass spectrometry. Our work identified a total of 94 DAPs between mock and pathogen treatment in WT and fld mutant. The DAPs were categorized into different functional groups along with their subcellular localization. The majority of DAPs are involved in metabolic processes and stress response. Among the subcellular compartments, plastids contained the highest number of DAPs, suggesting the importance of plastidic proteins in SAR activation. The findings of this study would provide resources to engineer efficient SAR activation traits in Arabidopsis and other plants.

Overexpression of Arabidopsis microRNA167 induces salicylic acid-dependent defense against Pseudomonas syringae through the regulation of its targets ARF6 and ARF8.

microRNAs are powerful regulators of growth, development, and stress responses in plants. The Arabidopsis thaliana microRNA miR167 was previously found to regulate diverse processes including flower development, root development, and response to osmotic stress by controlling the patterns of expression of its target genes AUXIN RESPONSE FACTOR 6 (ARF6), ARF8, and IAA‐Ala RESISTANT 3. Here, we report that miR167 also modulates defense against pathogens through ARF6 and ARF8. miR167 is differentially expressed in response to the bacterial pathogen Pseudomonas syringae, and overexpression of miR167 confers very high levels of resistance. This resistance appears to be due to suppression of auxin responses and is partially dependent upon salicylic acid signaling, and also depends upon altered stomatal behavior in these plants. Closure of stomata upon the detection of P. syringae is an important aspect of the basal defense response, as it prevents bacterial cells from entering the leaf interior and causing infection. Plants overexpressing miR167 constitutively maintain small stomatal apertures, resulting in very high resistance when the pathogen is inoculated onto the leaf surface. Additionally, the systemic acquired resistance (SAR) response is severely compromised in plants overexpressing miR167, in agreement with previous work showing that the activation of SAR requires intact auxin signaling responses. This work highlights a new role for miR167, and also emphasizes the importance of hormonal balance in short‐ and long‐term defense and of stomata as an initial barrier to pathogen entry.

Mechanisms formation of systemic acquired resistance in spring barley plants (<i>Hordeum vulgare</i> L.) during infection by the pathway of dark brown spot

The physiological and biochemical responses in spring barley plants to infection with a hemibiotrophic phytopathogenic fungus B. sorokiniana was studied. It was found that these responses of the plant organism are regulated by signaling pathways with the participation of the salicylic acid mediator (SA) and are associated with oxidative stress-localized accumulation of reactive oxygen molecules (ROS) in infected cells and/or neighboring cells. The activation of the microsomal fraction of NADPH oxidase isolated from barley leaves on days 1 and 3 after fungal infection was revealed, which is known to be responsible for the rapid formation of ROS in plant cells under the influence of fungal infection. At the same time, an increase in the activity of the peroxidase enzyme detoxifying ROS, in particular Н 2 О 2 , was observed in relation to the control (uninfected plants) by 1.6 and 2.2 times on the 1st and 3rd day after exposure, respectively. The inclusion of antioxidant defense mechanisms led to the stabilization of lipid peroxidation processes several days after infection. A reliable increase in the total content of water-soluble phenolic substances in the infected plant tissues was shown to have a protective effect on plants under stress, as well as an increase in the free pool of endogenous SA by 9 and 30 % during the first 24 hours and the next 3 days after infection, respectively. The data obtained indicate that endogenous S А is involved in the responses to infection of B. sorokiniana barley seedlings and is a necessary factor for the activation of SAR (systemic acquired resistance), which manifests itself in the accumulation of free S А and a decrease in its conjugated form in response to infection.

One- and Two-Proton Transfer Mechanisms Coexist in One Active Site.

Acibenzolar-S-methyl (ASM) is one of the most successfully commercialized plant activators of the systemic acquired resistance (SAR). However, its activation (hydrolysis) mechanism catalyzed by the salicylic acid binding protein 2 (SABP2) remains elusive. The fundamental catalytic mechanism of the SABP2-catalyzed hydrolysis of the ASM had been investigated by extensive computational and experimental studies, including QM/MM simulations, charge transfer analysis, small-molecule synthesis, and biochemical assays. Here we report that the promiscuous SABP2 shows different catalytic mechanisms toward different substrates. To catalyze the ASM hydrolysis, the SABP2 uses a two-proton transfer mechanism, and the key intermediate is stabilized by the charge transfer effect; to catalyze the ethyl 1,2,3-benzothiadiazole-7-carboxylate (BTM, an ASM analogue) hydrolysis, the SABP2 applies the one-proton transfer mechanism, and the classic tetrahedral intermediate is stabilized by the electrostatic effect. The HPLC analyses of the SABP2 esterase activities toward the ASM and the BTM show comparable results with our computaional results, suggesting that the obtained computational mechanism insights are reasonable. The obtained mechanism is not only an important supplement to the theory of enzymes' catalytic promiscuity, but it also contributes a possible strategy for the design of next generation plant SAR activators.

DORMANCY/AUXIN ASSOCIATED FAMILY PROTEIN 2 of Arabidopsis thaliana is a negative regulator of local and systemic acquired resistance.

To fine tune defense response output, plants recruit both positive and negative regulators. Here we report Arabidopsis DORMANCY/AUXIN ASSOCIATED FAMILY PROTEIN 2(DAP2) gene as a negative regulator of basal defense against virulent bacterial pathogens. Expression of DAP2 enhances upon pathogen inoculation. Our experiments show that DAP2 suppressed resistance against virulent strains of bacterial pathogens, pathogen-induced callose deposition, and ROS accumulation; however, it did not influence effector-triggered immunity. In addition, DAP2 negatively regulated systemic acquired resistance (SAR). DAP2 expression was enhanced in the pathogen-free systemic tissues of SAR-induced plants. Previously, Arabidopsis Flowering locus D (FLD) gene has been shown to be essential for SAR but not for local resistance. We show here that FLD function is necessary for SAR-induced expression of DAP2, suggesting DAP2 as a target of FLD for activation of SAR in Arabidopsis.

Management of Alternaria alternata of tomato (Lycopersicon esculentum Mill.) through SAR activators in natural conditions

The experiment was conducted at Department of Plant Pathology, S.K.N. College of Agriculture, Jobner (Rajasthan). Alternaria alternata was isolated from leaves of tomato and observed to be pathogenic under artificial conditions. It is cause heavy yield loss in rajasthan as well as in india. Among five systemic acquired resistance activators, salicylic acid was found most effective against Alternaria alternata in vivo conditions followed by, 2,4 Dichloroisonicotinic acid. All treatments as foilar spray were able to reduce disease severity over untreated control.

An engineered pathway for N-hydroxy-pipecolic acid synthesis enhances systemic acquired resistance in tomato.

Systemic acquired resistance (SAR) is a powerful immune response that triggers broad-spectrum disease resistance throughout a plant. In the model plant Arabidopsis thaliana, long-distance signaling and SAR activation in uninfected tissues occur without circulating immune cells and instead rely on the metabolite N-hydroxy-pipecolic acid (NHP). Engineering SAR in crop plants would enable external control of a plant's ability to mount a global defense response upon sudden changes in the environment. Such a metabolite-engineering approach would require the molecular machinery for producing and responding to NHP in the crop plant. Here, we used heterologous expression in Nicotiana benthamiana leaves to identify a minimal set of Arabidopsis genes necessary for the biosynthesis of NHP. Local expression of these genes in tomato leaves triggered SAR in distal tissues in the absence of a pathogen, suggesting that the SAR trait can be engineered to enhance a plant's endogenous ability to respond to pathogens. We also showed tomato produces endogenous NHP in response to a bacterial pathogen and that NHP is present across the plant kingdom, raising the possibility that an engineering strategy to enhance NHP-induced defenses could be possible in many crop plants.

Protocol: an improved method to quantify activation of systemic acquired resistance (SAR)

BackgroundPlant responses triggered upon detection of an invading pathogen include the generation of a number of mobile signals that travel to distant tissues and determine an increased resistance in distal, uninfected tissues, a defense response known as systemic acquired resistance (SAR). The more direct means of measuring activation of SAR by a primary local infection is the quantification of pathogen multiplication in distal, systemic sites of secondary infection. However, while such assay provides a biologically relevant quantification of SAR, it is hampered by experimental variation, requiring many repetitions for reliable results.ResultsWe propose a modification of the SAR assay based on the Arabidopsis–Pseudomonas syringae pathosystem exploiting the knowledge of source-sink relationships (orthostichies), known to centralize SAR-competency to upper leaves in the orthostichy of a lower primary infected leaf. Although many sources of variation such as genotypes of plant and pathogen, inoculation procedure, or environmental conditions are already taken into account to improve the performance of SAR assays, a strict leaf selection based on source-sink relationships is not usually implemented. We show how enacting this latter factor considerably improves data reliability, reducing the number of experimental repetitions for results.ConclusionsDirect selection of leaves for both primary and secondary inoculation exclusively within the orthostichy of the primary infected leaf is a key element on reducing the number of experimental repetitions required for statistically relevant SAR activation results.

A MPK3/6-WRKY33-ALD1-Pipecolic Acid Regulatory Loop Contributes to Systemic Acquired Resistance.

Plants induce systemic acquired resistance (SAR) upon localized exposure to pathogens. Pipecolic acid (Pip) production via AGD2-LIKE DEFENSE RESPONSE PROTEIN1 (ALD1) is key for SAR establishment. Here, we report a positive feedback loop important for SAR induction in Arabidopsis thaliana We showed that local activation of the MAP kinases MPK3 and MPK6 is sufficient to trigger Pip production and mount SAR. Consistent with this, mutations in MPK3 or MPK6 led to compromised Pip accumulation upon inoculation with the bacterial pathogen Pseudomonas syringae pv tomato DC3000 (Pto) AvrRpt2, which triggers strong sustained MAPK activation. By contrast, P. syringae pv maculicola and Pto, which induce transient MAPK activation, trigger Pip biosynthesis and SAR independently of MPK3/6. ALD1 expression, Pip accumulation, and SAR were compromised in mutants defective in the MPK3/6-regulated transcription factor WRKY33. Chromatin immunoprecipitation showed that WRKY33 binds to the ALD1 promoter. We found that Pip triggers activation of MPK3 and MPK6 and that MAPK activation after Pto AvrRpt2 inoculation is compromised in wrky33 and ald1 mutants. Collectively, our results reveal a positive regulatory loop consisting of MPK3/MPK6, WRKY33, ALD1, and Pip in SAR induction and suggest the existence of distinct SAR activation pathways that converge at the level of Pip biosynthesis.

Overexpression of NPR1 in Brassica juncea Confers Broad Spectrum Resistance to Fungal Pathogens.

Brassica juncea (Indian mustard) is a commercially important oil seed crop, which is highly affected by many biotic stresses. Among them, Alternaria leaf blight and powdery mildew are the most devastating diseases leading to huge yield losses in B. juncea around the world. In this regard, genetic engineering is a promising tool that may possibly allow us to enhance the B. juncea disease resistance against these pathogens. NPR1 (non-expressor of pathogen-related gene 1) is a bonafide receptor of salicylic acid (SA) which modulates multiple immune responses in plants especially activation of induced and systemic acquired resistance (SAR). Here, we report the isolation and characterization of new NPR1 homolog (BjNPR1) from B. juncea. The phylogenetic tree constructed based on the deduced sequence of BjNPR1 with homologs from other species revealed that BjNPR1 grouped together with other known NPR1 proteins of Cruciferae family, and was nearest to B. napus. Furthermore, expression analysis showed that BjNPR1 was upregulated after SA treatment and fungal infection but not by jasmonic acid or abscisic acid. To understand the defensive role of this gene, we generated B. juncea transgenic lines overexpressing BjNPR1, and further confirmed by PCR and Southern blotting. The transgenic lines showed no phenotypic abnormalities, and constitutive expression of BjNPR1 activates defense signaling pathways by priming the expression of antifungal PR genes. Moreover, BjNPR1 transgenic lines showed enhanced resistance to Alternaria brassicae and Erysiphe cruciferarum as there was delay in symptoms and reduced disease severity than non-transgenic plants. In addition, the rate of disease spreading to uninfected or distal parts was also delayed in transgenic plants thus suggesting the activation of SAR. Altogether, the present study suggests that BjNPR1 is involved in broad spectrum of disease resistance against fungal pathogens.

Arabidopsis thaliana GLUTATHIONE-S-TRANSFERASE THETA 2 interacts with RSI1/FLD to activate systemic acquired resistance.

A partly infected plant develops systemic acquired resistance (SAR) and shows heightened resistance during subsequent infections. The infected parts generate certain mobile signals that travel to the distal tissues and help to activate SAR. SAR is associated with epigenetic modifications of several defence-related genes. However, the mechanisms by which mobile signals contribute to epigenetic changes are little known. Previously, we have shown that the Arabidopsis REDUCED SYSTEMIC IMMUNITY 1 (RSI1, alias FLOWERING LOCUS D; FLD), which codes for a putative histone demethylase, is required for the activation of SAR. Here, we report the identification of GLUTATHIONE-S-TRANSFERASE THETA 2 (GSTT2) as an interacting factor of FLD. GSTT2 expression increases in pathogen-inoculated as well as pathogen-free distal tissues. The loss-of-function mutant of GSTT2 is compromised for SAR, but activates normal local resistance. Complementation lines of GSTT2 support its role in SAR activation. The distal tissues of gstt2 mutant plants accumulate significantly less salicylic acid (SA) and express a reduced level of the SA biosynthetic gene PAL1. In agreement with the established histone modification activity of FLD, gstt2 mutant plants accumulate an enhanced level of methylated and acetylated histones in the promoters of WRKY6 and WRKY29 genes. Together, these results demonstrate that GSTT2 is an interactor of FLD, which is required for SAR and SAR-associated epigenetic modifications.