A Defense Pathway Linking Plasma Membrane and Chloroplasts and Co-opted by Pathogens.

Chloroplasts are crucial players in the activation of defensive hormonal responses during plant-pathogen interactions. Here, we show that a plant virus-encoded protein re-localizes from the plasma membrane to chloroplasts upon activation of plant defense, interfering with the chloroplast-dependent anti-viral salicylic acid (SA) biosynthesis. Strikingly, we have found that plant pathogens from different kingdoms seem to have convergently evolved to target chloroplasts and impair SA-dependent defenses following an association with membranes, which relies on the co-existence of two subcellular targeting signals, an N-myristoylation site and a chloroplast transit peptide. This pattern is also present in plant proteins, at least one of which conversely activates SA defenses from the chloroplast. Taken together, our results suggest that a pathway linking plasma membrane to chloroplasts and activating defense exists in plants and that such pathway has been co-opted by plant pathogens during host-pathogen co-evolution to promote virulence through suppression of SA responses.

TIC236 gain-of-function mutations unveil the link between plastid division and plastid protein import.

SignificanceAlthough plastid division is critical for plant development, how components of the plastid division machinery (PDM) are imported into plastids remains unexplored. A forward genetic screen to identify suppressors of a crumpled leaf (crl) mutant deficient in plastid division led us to find dominant gain-of-function (GF) mutations in TIC236, which significantly increases the import of PDM components and completely rescues crl phenotypes. The defective plastid division phenotypes in crl and tic236-knockdown mutants and CRL-TIC236 association in a functional complex indicate that the CRL-TIC236 module is vital for plastid division. Hence, we report the first GF translocon mutants and unveil CRL as a novel functional partner of TIC236 for PDM import.

Antagonistic modules regulate photosynthesis-associated nuclear genes via GOLDEN2-LIKE transcription factors.

GOLDEN2-LIKE (GLK) transcription factors drive the expression of photosynthesis-associated nuclear genes (PhANGs) indispensable for chloroplast biogenesis. Salicylic acid (SA)-induced SIGMA FACTOR-BINDING PROTEIN 1 (SIB1), a transcription coregulator and positive regulator of cell death, interacts with GLK1 and GLK2 to reinforce the expression of PhANGs, leading to photoinhibition of photosystem II and singlet oxygen (1O2) burst in chloroplasts. 1O2 then contributes to SA-induced cell death via EXECUTER 1 (EX1; 1O2 sensor protein)-mediated retrograde signaling upon reaching a critical level. This earlier finding has initiated research on the potential role of GLK1/2 and EX1 in SA signaling. Consistent with this view, we reveal that LESION-SIMULATING DISEASE 1 (LSD1), a transcription coregulator and negative regulator of SA-primed cell death, interacts with GLK1/2 to repress their activities in Arabidopsis (Arabidopsis thaliana). Overexpression of LSD1 repressed GLK target genes, including PhANGs, whereas loss of LSD1 enhanced their expression. Remarkably, LSD1 overexpression inhibited chloroplast biogenesis, resembling the characteristic glk1glk2 double mutant phenotype. Subsequent chromatin immunoprecipitation coupled with expression analyses further revealed that LSD1 inhibits the DNA-binding activity of GLK1 toward its target promoters. SA-induced nuclear-targeted SIB1 proteins appeared to interrupt the LSD1-GLK interaction, and the subsequent SIB1-GLK interaction activated EX1-mediated 1O2 signaling, elucidating antagonistic modules SIB1 and LSD1 in the regulation of GLK activity. Taken together, we provide a working model that SIB1 and LSD1, mutually exclusive SA-signaling components, antagonistically regulate GLK1/2 to fine-tune the expression of PhANGs, thereby modulating 1O2 homeostasis and related stress responses.

FATTY ACID DESATURASE5 Is Required to Induce Autoimmune Responses in Gigantic Chloroplast Mutants of Arabidopsis.

Chloroplasts mediate genetically controlled cell death via chloroplast-to-nucleus retrograde signaling. To decipher the mechanism, we examined chloroplast-linked lesion-mimic mutants of Arabidopsis (Arabidopsis thaliana) deficient in plastid division, thereby developing gigantic chloroplasts (GCs). These GC mutants, including crumpled leaf (crl), constitutively express immune-related genes and show light-dependent localized cell death (LCD), mirroring typical autoimmune responses. Our reverse genetic approach excludes any potential role of immune/stress hormones in triggering LCD. Instead, transcriptome and in silico analyses suggest that reactive electrophile species (RES) generated via oxidation of polyunsaturated fatty acids (PUFAs) or lipid peroxidation-driven signaling may induce LCD. Consistent with these results, the one of the suppressors of crl, dubbed spcrl4, contains a causative mutation in the nuclear gene encoding chloroplast-localized FATTY ACID DESATURASE5 (FAD5) that catalyzes the conversion of palmitic acid (16:0) to palmitoleic acid (16:1). The loss of FAD5 in the crl mutant might attenuate the levels of RES and/or lipid peroxidation due to the reduced levels of palmitic acid-driven PUFAs, which are prime targets of reactive oxygen species. The fact that fad5 also compromises the expression of immune-related genes and the development of LCD in other GC mutants substantiates the presence of an intrinsic retrograde signaling pathway, priming the autoimmune responses in a FAD5-dependent manner.

PLANT NATRIURETIC PEPTIDE A and Its Putative Receptor PNP-R2 Antagonize Salicylic Acid-Mediated Signaling and Cell Death.

The plant stress hormone salicylic acid (SA) participates in local and systemic acquired resistance, which eventually leads to whole-plant resistance to bacterial pathogens. However, if SA-mediated signaling is not appropriately controlled, plants incur defense-associated fitness costs such as growth inhibition and cell death. Despite its importance, to date only a few components counteracting the SA-primed stress responses have been identified in Arabidopsis (Arabidopsis thaliana). These include other plant hormones such as jasmonic acid and abscisic acid, and proteins such as LESION SIMULATING DISEASE1, a transcription coregulator. Here, we describe PLANT NATRIURETIC PEPTIDE A (PNP-A), a functional analog to vertebrate atrial natriuretic peptides, that appears to antagonize the SA-mediated plant stress responses. While loss of PNP-A potentiates SA-mediated signaling, exogenous application of synthetic PNP-A or overexpression of PNP-A significantly compromises the SA-primed immune responses. Moreover, we identify a plasma membrane-localized receptor-like protein, PNP-R2, that interacts with PNP-A and is required to initiate the PNP-A-mediated intracellular signaling. In summary, our work identifies a peptide and its putative cognate receptor as counteracting both SA-mediated signaling and SA-primed cell death in Arabidopsis.

Salicylate and jasmonate intertwine in ROS-triggered chloroplast-to-nucleus retrograde signaling.

Plants, being sessile, are frequently exposed to environmental perturbations, affecting their sustenance and survival. In response, distinct inherent mechanisms emerged during plant evolution to deal with environmental stresses. Among various organelles, chloroplast plays an indispensable role in plant cells. Besides providing the site for photosynthesis and biosynthesis of many important primary and secondary metabolites, including hormones, chloroplasts also act as environmental sensors. Any environmental perturbation directly influences the photosynthetic electron transport chain, leading to excess accumulation of reactive oxygen species (ROS), causing oxidative damages to biomolecules in the vicinity. To prevent excess ROS accumulation and the consequent oxidative damages, the chloroplast activates retrograde signaling (RS) pathways to reprogramme nuclear gene expression, defining plant's response to stress. Based on levels and site of ROS accumulation, distinct biomolecules are oxidized, generating specific derivatives that act as genuine signaling molecules, triggering specific RS pathways to instigate distinctive responses, including growth inhibition, acclimation, and programmed cell death. Though various RS pathways independently modulate nuclear gene expression, they also implicate the defense hormone salicylic acid (SA) and oxylipins, including 12-oxo-phytodienoic acid (OPDA) and jasmonic acid (JA), by promoting their biosynthesis and utilizing them for intra- and intercellular communications. Several studies reported the involvement of both hormones in individual RS pathways, but the precise dissection of their activation and participation in a given RS pathway remains an enigma. The present review describes the current understanding of how SA and JA intertwine in ROS-triggered RS pathways. We have also emphasized the future perspectives for elucidating stress specificity and spatiotemporal accumulation of respective hormones in a given RS pathway.

Uncoupled Expression of Nuclear and Plastid Photosynthesis-Associated Genes Contributes to Cell Death in a Lesion Mimic Mutant.

Chloroplast-to-nucleus retrograde signaling is essential for the coupled expression of photosynthesis-associated nuclear genes (PhANGs) and plastid genes (PhAPGs) to ensure the functional status of chloroplasts (Cp) in plants. Although various signaling components involved in the process have been identified in Arabidopsis (Arabidopsis thaliana), the biological relevance of such coordination remains an enigma. Here, we show that the uncoupled expression of PhANGs and PhAPGs contributes to the cell death in the lesion simulating disease1 (lsd1) mutant of Arabidopsis. A daylength-dependent increase of salicylic acid (SA) appears to rapidly up-regulate a gene encoding SIGMA FACTOR BINDING PROTEIN1 (SIB1), a transcriptional coregulator, in lsd1 before the onset of cell death. The dual targeting of SIB1 to the nucleus and the Cps leads to a simultaneous up-regulation of PhANGs and down-regulation of PhAPGs. Consequently, this disrupts the stoichiometry of photosynthetic proteins, especially in PSII, resulting in the generation of the highly reactive species singlet oxygen (1O2) in Cps. Accordingly, inactivation of the nuclear-encoded Cp protein EXECUTER1, a putative 1O2 sensor, significantly attenuates the lsd1-conferred cell death. Together, these results provide a pathway from the SA- to the 1O2-signaling pathway, which are intertwined via the uncoupled expression of PhANGs and PhAPGs, contributing to the lesion-mimicking cell death in lsd1.

Seed priming with brassinolides improves growth and reinforces antioxidative defenses under normal and heat stress conditions in seedlings of Brassica juncea.

Environmental stresses pose a major challenge for plant researchers to fulfill increasing food demand. Researchers are trying to generate high-yielding and stress-tolerant or resistant varieties using classical genetics and modern gene-editing tools; however, both approaches have limitations. Chemical treatments emerged as an alternative to improve yield and impart stress resilience. Brassinosteroids (BRs) are a group of phytohormones that regulate various biological processes, including stress management. With foliar spray methods, BR treatments showed promising results but are not economically feasible. We hypothesize that priming of seeds, which requires lesser amounts of BRs, could be equally effective in promoting growth and stress tolerance. Owing to this notion, we analyzed the impact of priming seeds with selected BRs, namely, 24-epibrassinolide (EBL) and 28-homobrassinolide (HBL), in Brassica juncea under normal and heat shock stress conditions. Seeds primed with BRs and grown until seedlings stage at normal conditions (20°C) were subjected to a heat shock (35°C) for a few hours, relating to what plants experience in natural conditions. Heat shock reduced the growth and biomass with an increased accumulation of reactive oxygen species. As anticipated, BRs treatments significantly improved the growth and physiological parameters with an enhanced antioxidant defense under both conditions. Transcriptional analyses revealed that BRs concomitantly induce growth and oxidative stress-responsive gene expression via the canonical BR-signaling pathway. Transfer of unstressed and heat-shock-treated seedlings to field conditions demonstrated the long-term effectivity of BR-priming. Our results showed seed priming with BRs could improve growth and resilience against heat shock; hence, it appears to be a viable strategy to enhance crop yields and stress tolerance.

The Arabidopsis CRUMPLED LEAF protein, a homolog of the cyanobacterial bilin lyase, retains the bilin-binding pocket for a yet unknown function.

The photosynthetic bacterial phycobiliprotein lyases, also called CpcT lyases, catalyze the biogenesis of phycobilisome, a light-harvesting antenna complex, through the covalent attachment of chromophores to the antenna proteins. The Arabidopsis CRUMPLED LEAF (CRL) protein is a homolog of the cyanobacterial CpcT lyase. Loss of CRL leads to multiple lesions, including localized foliar cell death, constitutive expression of stress-related nuclear genes, abnormal cell cycle, and impaired plastid division. Notwithstanding the apparent phenotypes, the function of CRL still remains elusive. To gain insight into the function of CRL, we examined whether CRL still retains the capacity to bind with the bacterial chromophore phycocyanobilin (PCB) and its plant analog phytochromobilin (PΦB). The revealed structure of the CpcT domain of CRL is comparable to that of the CpcT lyase, despite the low sequence identity. The subsequent in vitro biochemical assays found, as shown for the CpcT lyase, that PCB/PΦB binds to the CRL dimer. However, some mutant forms of CRL, substantially compromised in their bilin-binding ability, still restore the crl-induced multiple lesions. These results suggest that although CRL retains the bilin-binding pocket, it seems not functionally associated with the crl-induced multiple lesions.

N-Terminal Acetylation Stabilizes SIGMA FACTOR BINDING PROTEIN1 Involved in Salicylic Acid-Primed Cell Death.

N-terminal (Nt) acetylation (NTA) is an ample and irreversible cotranslational protein modification catalyzed by ribosome-associated Nt-acetyltransferases. NTA on specific proteins can act as a degradation signal (called an Ac/N-degron) for proteolysis in yeast and mammals. However, in plants, the biological relevance of NTA remains largely unexplored. In this study, we reveal that Arabidopsis (Arabidopsis thaliana) SIGMA FACTOR-BINDING PROTEIN1 (SIB1), a transcription coregulator and a positive regulator of salicylic acid-primed cell death, undergoes an absolute NTA on the initiator Met; Nt-acetyltransferase B (NatB) partly contributes to this modification. While NTA results in destabilization of certain target proteins, our genetic and biochemical analyses revealed that plant NatB-involved NTA instead renders SIB1 more stable. Given that the ubiquitin/proteasome system stimulates SIB1 degradation, it seems that the NTA-conferred stability ensures the timely expression of SIB1-dependent genes, mostly related to immune responses. Taking our findings together, here we report a noncanonical NTA-driven protein stabilization in land plants.

Impaired PSII Proteostasis Promotes Retrograde Signaling via Salicylic Acid.

Photodamage of the PSII reaction center (RC) is an inevitable process in an oxygen-rich environment. The damaged PSII RC proteins (Dam-PSII) undergo degradation via the thylakoid membrane-bound FtsH metalloprotease, followed by posttranslational assembly of PSII. While the effect of Dam-PSII on gene regulation is described for cyanobacteria, its role in land plants is largely unknown. In this study, we reveal an intriguing retrograde signaling pathway by using the Arabidopsis (Arabidopsis thaliana) yellow variegated2-9 mutant, which expresses a mutated FtsH2 (FtsH2G267D) metalloprotease, specifically impairing its substrate-unfolding activity. This lesion leads to the perturbation of PSII protein homeostasis (proteostasis) and the accumulation of Dam-PSII. Subsequently, this results in an up-regulation of salicylic acid (SA)-responsive genes, which is abrogated by inactivation of either an SA transporter in the chloroplast envelope membrane or extraplastidic SA signaling components as well as by removal of SA. These results suggest that the stress hormone SA, which is mainly synthesized via the chloroplast isochorismate pathway in response to the impaired PSII proteostasis, mediates the retrograde signaling. These findings reinforce the emerging view of chloroplast function toward plant stress responses and suggest SA as a potential plastid factor mediating retrograde signaling.

Impaired PSII proteostasis triggers a UPR-like response in the var2 mutant of Arabidopsis.

Cellular protein homeostasis (proteostasis) is maintained through the balance between de novo synthesis and proteolysis. The unfolded/misfolded protein response (UPR) that is triggered by stressed endoplasmic reticulum (ER) also plays an important role in proteostasis in both plants and animals. Although ER-triggered UPR has been extensively studied in plants, the molecular mechanisms underlying mitochondrial and chloroplastic UPRs are largely uncharacterized despite the fact that these organelles are sites of production of harmful reactive oxygen species (ROS), which damage proteins. In this study, we demonstrate that chloroplasts of the Arabidopsis yellow leaf variegation 2 (var2) mutant, which lacks the metalloprotease FtsH2, accumulate damaged chloroplast proteins and trigger a UPR-like response, namely the accumulation of a suite of chloroplast proteins involved in protein quality control (PQC). These PQC proteins include heat-shock proteins, chaperones, proteases, and ROS detoxifiers. Given that FtsH2 functions primarily in photosystem II proteostasis, the accumulation of PQC-related proteins may balance the FtsH2 deficiency. Moreover, the apparent up-regulation of the cognate transcripts indicates that the accumulation of PQC-related proteins in var2 is probably mediated by retrograde signaling, indicating the occurrence of a UPR-like response in var2.

Singlet oxygen- and EXECUTER1-mediated signaling is initiated in grana margins and depends on the protease FtsH2.

Formation of singlet oxygen ((1)O2) has been implicated with damaging photosystem II (PSII) that needs to undergo continuous repair to maintain photosynthetic electron transport. In addition to its damaging effect, (1)O2 has also been shown to act as a signal that triggers stress acclimation and an enhanced stress resistance. A signaling role of (1)O2 was first documented in the fluorescent (flu) mutant of Arabidopsis It strictly depends on the chloroplast protein EXECUTER1 (EX1) and happens under nonphotoinhibitory light conditions. Under severe light stress, signaling is initiated independently of EX1 by (1)O2 that is thought to be generated at the acceptor side of active PSII within the core of grana stacks. The results of the present study suggest a second source of (1)O2 formation in grana margins close to the site of chlorophyll synthesis where EX1 is localized and the disassembly of damaged and reassembly of active PSII take place. The initiation of (1)O2 signaling in grana margins depends on EX1 and the ATP-dependent zinc metalloprotease FtsH. As FtsH cleaves also the D1 protein during the disassembly of damaged PSII, EX1- and (1)O2-mediated signaling seems to be not only spatially but also functionally associated with the repair of PSII.

Singlet oxygen-triggered chloroplast-to-nucleus retrograde signalling pathways: An emerging perspective.

Singlet oxygen (1 O2 ) is a prime cause of photo-damage of the photosynthetic apparatus. The chlorophyll molecules in the photosystem II reaction center and in the light-harvesting antenna complex are major sources of 1 O2 generation. It has been thought that the generation of 1 O2 mainly takes place in the appressed regions of the thylakoid membranes, namely, the grana core, where most of the active photosystem II complexes are localized. Apart from being a toxic molecule, new evidence suggests that 1 O2 significantly contributes to chloroplast-to-nucleus retrograde signalling that primes acclimation and cell death responses. Interestingly, recent studies reveal that chloroplasts operate two distinct 1 O2 -triggered retrograde signalling pathways in which ß-carotene and a nuclear-encoded chloroplast protein EXECUTER1 play essential roles as signalling mediators. The coexistence of these mediators raises several questions: their crosstalk, source(s) of 1 O2 , downstream signalling components, and the perception and reaction mechanism of these mediators towards 1 O2 . In this review, we mainly discuss the molecular genetic basis of the mode of action of these two putative 1 O2 sensors and their corresponding retrograde signalling pathways. In addition, we also propose the possible existence of an alternative source of 1 O2 , which is spatially and functionally separated from the grana core.

Xyloglucan endo-transglycosylase/hydrolase (XET/H) gene is expressed during the seed germination in Podophyllum hexandrum: a high altitude Himalayan plant.

MAIN CONCLUSION: Xyloglucan endo-transglycosylase/hydrolase ( Ph XET/H) regulates Podophyllum seed germination via GA mediated up-accumulation of Ph XET protein and subsequent endosperm weakening. Xyloglucan endo-transglycosylase/hydrolase (XET/H) belong to glycosyl hydrolase family 16, which play an important role in endosperm weakening and embryonic expansion during seed germination. Podophyllum hexandrum is a high altitude medicinal plant exploited for its etoposides which are potential anticancer compounds. During seed germination in Podophyllum, accumulation of XET/H transcripts was recorded. This data confirmed its possible role in determining the fate of seed for germination. Full length cDNA of a membrane bound XET/H (here onwards PhXET) was cloned from the germinating seeds of Podophyllum. Analysis of nucleotide sequence revealed PhXET with an open reading frame of 720 bp encoding a protein of 239 amino acids with a molecular mass of 28 kDa and pI of 7.58. In silico structure prediction of PhXET showed homology with that of Populus tremula (1UN1). PhXET was predicted to have a potential GPI-anchor domain and was located in plasma membrane. It was found that the exogenously applied phytohormones (GA and ABA) regulate the expression of PhXET. The obtained data showed that the PhXET regulates seed germination in Podophyllum by supplementing its activity along with other endosperm weakening and embryo expansion genes.

In vitro flowering associated protein changes in Dendrocalamus hamiltonii.

In Dendrocalamus hamiltonii, conversion of vegetative meristem to a floral meristem was successfully achieved on flower induction medium. A total of 128 differentially expressed proteins were evidenced by 2DE in floral meristem protein profiles. Analysis of 103 proteins through PMF revealed change in abundance in the content of 79 proteins, disappearance and new appearance in the content of 7 and 17 proteins, respectively. MS/MS and subsequent homology search identified 65 proteins that were involved in metabolism (22 proteins), regulatory (11 proteins), signaling and transportation (12 proteins), stress (6 proteins), flowering (8 proteins), and unknown functions (6 proteins). The data suggested that change in metabolism related proteins might be providing nutrient resources for floral initiation in D. hamiltonii. Further, interactive effects of various proteins like bHLH145, B-4c transcription factors (heat stress transcription factor), maturase K, MADS box, zinc finger proteins, and scarecrow-like protein 21 (flowering related), a key enzyme of ethylene biosynthesis SAMS (S-adenosylmethionine synthase) and aminocyclopropane-1-carboxylate synthase, improved calcium signaling related proteins (CML36), and change in phytohormone related proteins such as phosphatase proteins (2c3 and 2c55), which are the positive regulators of gibberellic acid and phytochrome regulation related proteins (DASH, LWD1) might be the possible major regulators of floral transition in this bamboo.

Plant proteomics in India and Nepal: current status and challenges ahead.

Plant proteomics has made tremendous contributions in understanding the complex processes of plant biology. Here, its current status in India and Nepal is discussed. Gel-based proteomics is predominantly utilized on crops and non-crops to analyze majorly abiotic (49 %) and biotic (18 %) stress, development (11 %) and post-translational modifications (7 %). Rice is the most explored system (36 %) with major focus on abiotic mainly dehydration (36 %) stress. In spite of expensive proteomics setup and scarcity of trained workforce, output in form of publications is encouraging. To boost plant proteomics in India and Nepal, researchers have discussed ground level issues among themselves and with the International Plant Proteomics Organization (INPPO) to act in priority on concerns like food security. Active collaboration may help in translating this knowledge to fruitful applications.

Improving photosynthetic efficiency by modulating non-photochemical quenching.

High light exposure rapidly activates non-photochemical quenching (NPQ), protecting plants from photooxidative damage. Contrarily, its relaxation upon transition to normal light occurs quite slowly, limiting photosynthetic efficiency. De Souza et al. demonstrated that by overexpressing NPQ-related genes, faster NPQ relaxation and enhanced photosynthesis can be achieved under fluctuating light conditions.

Endosperm: thermal sensor and regulator of seed thermoinhibition.

Seed thermoinhibition protects emerging seedlings from thermodamage by preventing seed germination at elevated temperatures. It had remained unknown how a seed fine-tunes its germination in response to temperature. Recently, Piskurewicz et al. demonstrated that endosperm phyB senses increased temperature, thereby facilitating PIF3-mediated abscisic acid (ABA) accumulation to inhibit germination and embryo elongation.

Jasmonic acid limits Rhizoctonia solani AG1-IA infection in rice by modulating reactive oxygen species homeostasis.

Sheath blight disease of rice caused by a soil-borne fungal pathogen Rhizoctonia solani AG1-IA is one of the major threats to rice production globally. During host-pathogen interactions, reactive oxygen species (ROS) play an important role in pathogen virulence and plant defense. For example, necrotrophic pathogens induce ROS production to damage host cells, whereas the host can incite ROS to kill the pathogen. From the host perspective, it is essential to understand how the antioxidant machinery maintains a delicate balance of ROS to protect itself from its lethal effects. Here, we investigated the pathogen-induced accumulation of ROS and implicated damage in two rice genotypes (PR114, susceptible; ShB, moderately tolerant) varying in the level of susceptibility to R. solani AG1-IA. Compared to PR114, ShB exhibited a better antioxidant response and reasonably lesser oxidative damage. Further, we observed elevated levels of jasmonic acid (JA) in ShB, which was otherwise decreased in PR114 in response to pathogen infection. As depicted, an elevated level of JA was in agreement with the expression profiles of genes involved in its biosynthesis and signaling. To further ascertain if the heightened antioxidant response is JA-dependent or independent, methyl jasmonate (MeJA) was exogenously applied to PR114, and antioxidant response in terms of gene expression, enzyme activities, and oxidative damage was studied in R. solani infected samples. Surprisingly, the exogenous application of MeJA complemented the antioxidant response and reduced oxidative damage in PR114, thus suggesting that the antioxidant defense system is under transcriptional control of JA.