Trichoderma asperellum xylanases promote growth and induce resistance in poplar.

Xylanase secreted by Trichoderma asperellum ACCC30536 can stimulate the systemic resistance of host plants against pathogenic fungi. Following T. asperellum conidia co-culture with Populus davidiana × P. alba var. pyramidalis Louche (PdPap) seedlings, the expression of xylanases TasXyn29.4 and TasXyn24.2 in T. asperellum were upregulated, peaking at 12 h, by 106 (26.74) and 10.1 (23.34)-fold compared with the control, respectively. However, the expression of TasXyn24.4 and TasXyn24.0 was not detected. When recombinant xylanases rTasXyn29.4 and rTasXyn24.2 were heterologously expressed in Pichia pastoris GS115, their activities reached 18.9 IU/mL and 20.4 IU/mL, respectively. In PdPap seedlings induced by rTasXyn29.4 and rTasXyn24.2, the auxin and jasmonic acid signaling pathways were activated to promote growth and enhance resistance against pathogens. PdPap seedlings treated with both xylanases showed increased methyl jasmonate contents at 12 hpi, reaching 122 % (127 µg/g) compared with the control. However, neither of the xylanases could induce the salicylic acid signaling pathway in PdPap seedlings. Meanwhile, both xylanases could enhance the antioxidant ability of PdPap seedlings by improving their catalase activity. Both xylanases significantly induced systemic resistance of PdPap seedlings against Alternaria alternata, Rhizoctonia solani, and Fusarium oxysporum. However, the xylanases could only be sensed by the roots of the PdPap seedlings, not the leaves. In summary, rTasXyn29.4 and rTasXyn24.2 from T. asperellum ACCC30536 promoted growth and induced systemic resistance of PdPap seedlings, which endowed the PdPap seedlings broad-spectrum resistance to phytopathogens.

Simultaneous detection of plant growth regulators jasmonic acid and methyl jasmonate in plant samples by a monoclonal antibody-based ELISA.

Methyl jasmonate (MeJA) and its free-acid form, jasmonic acid (JA), collectively referred to as jasmonates (JAs), are natural plant growth regulators that are widely present in higher plants. Simultaneous detection of JA and MeJA in plant samples is of significance and is a great challenging issue. In this study, coupling with two extraction methods, a sensitive monoclonal antibody (mAb) based enzyme-linked immunosorbent assay (ELISA) for simultaneous detection of JA and MeJA in plant samples was developed. The JA-bovine serum albumin (BSA) conjugate was used as an immunogen for the production of mAb. As the produced mAb exhibited higher recognition ability towards MeJA than towards JA, ELISA was established using MeJA as the standard. Under optimal experimental conditions, the IC50 and LOD values of ELISA for MeJA were 2.02 ng mL-1 and 0.20 ng mL-1, respectively. In the first extraction method, MeJA in plant samples was evaporated and only JA was extracted. In the second extraction method, both JA and MeJA were extracted. After methylation, JA in the extracts was converted into MeJA, and the whole MeJA in the extracts was measured by ELISA. Plant samples including the leaves of Salvia splendens, the flowers of Salvia splendens and the fruit of grapes were collected. JA and MeJA in these samples were detected by the proposed ELISA. It was found that the concentrations of JA in these three plant samples were about 3-5 times higher than those of MeJA in those samples. ELISA was also confirmed by HPLC. There was a good correlation between ELISA and HPLC.

Early Pep-13-induced immune responses are SERK3A/B-dependent in potato.

Potato plants treated with the pathogen-associated molecular pattern Pep-13 mount salicylic acid- and jasmonic acid-dependent defense responses, leading to enhanced resistance against Phytophthora infestans, the causal agent of late blight disease. Recognition of Pep-13 is assumed to occur by binding to a yet unknown plasma membrane-localized receptor kinase. The potato genes annotated to encode the co-receptor BAK1, StSERK3A and StSERK3B, are activated in response to Pep-13 treatment. Transgenic RNAi-potato plants with reduced expression of both SERK3A and SERK3B were generated. In response to Pep-13 treatment, the formation of reactive oxygen species and MAP kinase activation, observed in wild type plants, is highly reduced in StSERK3A/B-RNAi plants, suggesting that StSERK3A/B are required for perception of Pep-13 in potato. In contrast, defense gene expression is induced by Pep-13 in both control and StSERK3A/B-depleted plants. Altered morphology of StSERK3A/B-RNAi plants correlates with major shifts in metabolism, as determined by untargeted metabolite profiling. Enhanced levels of hydroxycinnamic acid amides, typical phytoalexins of potato, in StSERK3A/B-RNAi plants are accompanied by significantly decreased levels of flavonoids and steroidal glycoalkaloids. Thus, altered metabolism in StSERK3A/B-RNAi plants correlates with the ability of StSERK3A/B-depleted plants to mount defense, despite highly decreased early immune responses.

Uptake of pharmaceuticals acts as an abiotic stress and triggers variation of jasmonates in Malabar spinach (Basella alba. L).

In recent years, pharmaceuticals have received increasing attentions because of their potential risks to the environment, but researches focusing on their impacts on defense system of living plants are still lacking. As an important class of phytohormones, jasmonates play crucial roles in plant defense system against environmental stress. In order to investigate the effect of pharmaceuticals uptake on endogenous jasmonates, an in vivo solid phase microextraction (SPME) method was established to simultaneously detect and monitor both pharmaceuticals and jasmonates in living plants. The proposed method exhibited wide linear ranges, high sensitivity (limits of detection ranging 0.0043-0.035 ng g-1 for pharmaceuticals and 0.091-0.22 ng g-1 for jasmonates, respectively), and satisfactory reproducibility (relative standard deviation of intrafiber ranging 4.2%-8.6% and interfiber ranging 5.2%-8.2%, respectively). Subsequently, this method was successfully applied to track the concentrations of each pharmaceutical and corresponding jasmonates in living Malabar spinach plants (Basella alba. L) exposed to three common pharmaceuticals (i.e. gemfibrozil, mefenamic acid and tolfenamic acid) over 15 days. In result, all pharmaceuticals appeared to trigger intensive biosynthesis of jasmonic acid (JA) (3.1-9.4 times of control) while reduced the concentration of methyl jasmonate (MeJA) (18.3%-38.1% of control). We inferred that uptake of pharmaceuticals acted as an abiotic stress and stimulated the plant defense response because of the variation of jasmonates. To the best of our knowledge, this is the first study applying SPME to detect and track both pharmaceuticals and phytohormones in living plants, which not only provided a glimpse to the adverse effect of pharmaceuticals on plants as well as the regulation of endogenous jasmonates, but also set a promising template for future in vivo analysis of xenobiotics and plant endogenous substances.

Gene networks underlying the early regulation of Paraburkholderia phytofirmans PsJN induced systemic resistance in Arabidopsis.

Plant defense responses to biotic stresses are complex biological processes, all governed by sophisticated molecular regulations. Induced systemic resistance (ISR) is one of these defense mechanisms where beneficial bacteria or fungi prime plants to resist pathogens or pest attacks. In ISR, the defense arsenal in plants remains dormant and it is only triggered by an infection, allowing a better allocation of plant resources. Our group recently described that the well-known beneficial bacterium Paraburkholderia phytofirmans PsJN is able to induce Arabidopsis thaliana resistance to Pseudomonas syringae pv. tomato (Pst) DC3000 through ISR, and that ethylene, jasmonate and salicylic acid are involved in this protection. Nevertheless, the molecular networks governing this beneficial interaction remain unknown. To tackle this issue, we analyzed the temporal changes in the transcriptome of PsJN-inoculated plants before and after being infected with Pst DC3000. These data were used to perform a gene network analysis to identify highly connected transcription factors. Before the pathogen challenge, the strain PsJN regulated 405 genes (corresponding to 1.8% of the analyzed genome). PsJN-inoculated plants presented a faster and stronger transcriptional response at 1-hour post infection (hpi) compared with the non-inoculated plants, which presented the highest transcriptional changes at 24 hpi. A principal component analysis showed that PsJN-induced plant responses to the pathogen could be differentiated from those induced by the pathogen itself. Forty-eight transcription factors were regulated by PsJN at 1 hpi, and a system biology analysis revealed a network with four clusters. Within these clusters LHY, WRKY28, MYB31 and RRTF1 are highly connected transcription factors, which could act as hub regulators in this interaction. Concordantly with our previous results, these clusters are related to jasmonate, ethylene, salicylic, acid and ROS pathways. These results indicate that a rapid and specific response of PsJN-inoculated plants to the virulent DC3000 strain could be the pivotal element in the protection mechanism.

Melatonin Induces Disease Resistance to Botrytis cinerea in Tomato Fruit by Activating Jasmonic Acid Signaling Pathway.

Melatonin acts as a crucial signaling molecule with multiple physiological functions in plant response to abiotic and biotic stresses. However, the impact and regulatory mechanism of melatonin on attenuating tomato fruit fungal decay are unclear. In this study, we investigated the potential roles of melatonin in modulating fruit resistance to Botrytis cinerea and explored related physiological and molecular mechanisms. The results revealed that disease resistance was strongly enhanced by melatonin treatment, and 50 µM was confirmed as the best concentration. Melatonin treatment increased the activities of defense-related enzymes and decreased hydrogen peroxide (H2O2) content with enhanced antioxidant enzyme activities. Moreover, we found that melatonin treatment increased methyl jasmonate (MeJA) content; up-regulated the expressions of SlLoxD, SlAOC, and SlPI II; and reduced the expressions of SlMYC2 and SlJAZ1. We postulated that melatonin played a positive role in tomato fruit resistance to Botrytis cinerea through regulating H2O2 level and JA signaling pathway.

Ethylene Perception Is Associated with Methyl-Jasmonate-Mediated Immune Response against Botrytis cinerea in Tomato Fruit.

Jasmonic acid (JA)- and ethylene-mediated signaling pathways are reported to have synergistic effects on inhibiting gray mold. The present study aimed to explain the role of ethylene perception in methyl jasmonate (MeJA)-mediated immune responses. Results showed that exogenous MeJA enhanced disease resistance, accompanied by the induction of endogenous JA biosynthesis and ethylene production, which led to the activation of the phenolic metabolism pathway. Blocking ethylene perception using 1-methylcyclopropene (1-MCP) either before or after MeJA treatment could differently weaken the disease responses induced by MeJA, including suppressing the induction of ethylene production and JA contents and reducing activities of lipoxygenase and allene oxide synthase compared to MeJA treatment alone. Consequently, MeJA-induced elevations in the total phenolic content and the activities of phenylalanine ammonia-lyase, cinnamate 4-hydroxylase, 4-coumarate:coenzyme A ligase, and peroxidase were impaired by 1-MCP. These results suggested that ethylene perception participated in MeJA-mediated immune responses in tomato fruit.

Jasmonate signalling in carnivorous plants: copycat of plant defence mechanisms.

The lipid-derived jasmonate phytohormones (JAs) regulate a wide spectrum of physiological processes in plants such as growth, development, tolerance to abiotic stresses, and defence against pathogen infection and insect attack. Recently, a new role for JAs has been revealed in carnivorous plants. In these specialized plants, JAs can induce the formation of digestive cavities and regulate enzyme production in response to different stimuli from caught prey. Appearing to be a new function for JAs in plants, a closer look reveals that the signalling pathways involved resemble known signalling pathways from plant defence mechanisms. Moreover, the digestion-related secretome of carnivorous plants is composed of many pathogenesis-related (PR) proteins and low molecular weight compounds, indicating that the plant carnivory syndrome is related to and has evolved from plant defence mechanisms. This review describes the similarities between defence and carnivory. It further describes how, after recognition of caught insects, JAs enable the carnivorous plants to digest and benefit from the prey. In addition, a causal connection between electrical and jasmonate signalling is discussed.

Hydrophobin HFBII-4 from Trichoderma asperellum induces antifungal resistance in poplar.

Herein, the class II hydrophobin gene HFBII-4 was cloned from the biocontrol agent Trichoderma asperellum ACCC30536 and recombinant rHFBII-4 was expressed in Pichia pastoris GS115. Treatment of Populus davidiana × P. alba var. pyramidalis (PdPap poplar) with rHFBII-4 altered the expression levels of genes in the auxin, salicylic acid (SA), and jasmonic acid (JA) signal transduction pathways. Polyphenol oxidase (PPO) and phenylalanine ammonia lyase (PAL) enzyme activities were induced with rHFBII-4. Evans Blue and nitro blue tetrazolium (NBT) staining indicated that cell membrane permeability and reactive oxygen species were lower in the leaves of plants treated with rHFBII-4. The chlorophyll content was higher than that of control at 2-5 days after treatment. Furthermore, poplar seedlings were inoculated with Alternaria alternata, disease symptoms were observed. The diseased area was smaller in leaves induced with rHFBII-4 compared with control. In summary, rHFBII-4 enhances resistance to A. alternata.

Transcriptomic and Phytochemical Analyses Reveal Root-Mediated Resource-Based Defense Response to Leaf Herbivory by Ectropis oblique in Tea Plant ( Camellia sinensis).

Leaf herbivory on tea plants ( Camellia sinensis) by tea geometrids ( Ectropis oblique) severely threaten the yield and quality of tea. In previous work, we found that local defense response was induced in damaged leaves by geometrids at the transcriptome level. Here, we investigated the systemic response triggered in undamaged roots and the potential role of roots in response to leaf herbivory. Comparative transcriptome analysis and carbohydrate dynamics indicated that leaf herbivory activated systemic carbon reallocation to enhance resource investment for local secondary metabolism. The crucial role of jasmonic acid and the involvement of other potential hormone signals for local and systemic signaling networks were supported by phytohormone quantification and dynamic expression analysis of phytohormone-related genes. This work represents a deep understanding of the interaction of tea plants and geometrids from the perspective of systems biology and reveals that tea plants have evolved an intricate root-mediated resource-based resistance strategy to cope with geometrid attack.

Transcriptome analysis of an incompatible Persea americana-Phytophthora cinnamomi interaction reveals the involvement of SA- and JA-pathways in a successful defense response.

Phytophthora cinnamomi Rands (Pc) is a hemibiotrophic oomycete and the causal agent of Phytophthora root rot (PRR) of the commercially important fruit crop avocado (Persea americana Mill.). Plant defense against pathogens is modulated by phytohormone signaling pathways such as salicylic acid (SA), jasmonic acid (JA), ethylene (ET), auxin and abscisic acid. The role of specific signaling pathways induced and regulated during hemibiotroph-plant interactions has been widely debated. Some studies report SA mediated defense while others hypothesize that JA responses restrict the spread of pathogens. This study aimed to identify the role of SA- and JA- associated genes in the defense strategy of a resistant avocado rootstock, Dusa in response to Pc infection. Transcripts associated with SA-mediated defense pathways and lignin biosynthesis were upregulated at 6 hours post-inoculation (hpi). Results suggest that auxin, reactive oxygen species (ROS) and Ca2+ signaling was also important during this early time point, while JA signaling was absent. Both SA and JA defense responses were shown to play a role during defense at 18 hpi. Induction of genes associated with ROS detoxification and cell wall digestion (ß-1-3-glucanase) was also observed. Most genes induced at 24 hpi were linked to JA responses. Other processes at play in avocado at 24 hpi include cell wall strengthening, the formation of phenolics and induction of arabinogalactan, a gene linked to Pc zoospore immobility. This study represents the first transcriptome wide analysis of a resistant avocado rootstock treated with SA and JA compared to Pc infection. The results provide evidence of a biphasic defense response against the hemibiotroph, which initially involves SA-mediated gene expression followed by the enrichment of JA-mediated defense from 18 to 24 hpi. Genes and molecular pathways linked to Pc resistance are highlighted and may serve as future targets for manipulation in the development of PRR resistant avocado rootstocks.

Jasmonic acid-induced plant defenses delay caterpillar developmental resistance to a baculovirus: Slow-growth, high-mortality hypothesis in plant-insect-pathogen interactions.

Plants damaged by herbivore feeding can induce defensive responses that reduce herbivore growth. The slow-growth, high-mortality hypothesis postulates that these non-lethal plant defenses prolong the herbivore's period of susceptibility to natural enemies, such as predators and parasitoids. While many juvenile animals increase their disease resistance as they grow, direct tests of the slow-growth, high-mortality hypothesis in the context of plant-herbivore-pathogen interactions are lacking. Caterpillars increase their resistance to lethal baculoviruses as they develop within and across instars, a phenomenon termed developmental resistance. Progression of developmental resistance can occur through age-related increases in systemic immune functioning and/or midgut-based resistance. Here, we examined the slow-growth, high-mortality hypothesis in the context of developmental resistance of caterpillars to baculoviruses. Intra-stadial (within-instar) developmental resistance of the fall armyworm, Spodoptera frugiperda, to an oral inoculum of the baculovirus SfMNPV increased more rapidly with age when larvae were fed on non-induced foliage than foliage that was induced by jasmonic acid (a phytohormone that up-regulates plant anti-herbivore defenses). The degree of developmental resistance observed was attributable to larval weight at the time of virus inoculation. Thus, slower growth on induced plants prolonged the window of larval susceptibility to the baculovirus. Developmental resistance on induced and non-induced plants was absent when budded virus was injected intrahemocoelically bypassing the midgut, suggesting that developmental resistance was gut-based. Addition of fluorescent brightener, which weakens midgut-based resistance mechanisms to oral virus challenge, abolished developmental resistance. These results highlight the impact of plant defenses on herbivore growth rate and consequences for disease risk.

CRISPR/Cas9-Mediated Immunity in Plants Against Pathogens.

Global crop production is highly threatened due to pathogen invasion. The huge quantity of pesticides application, although harmful to the environment and human health, is carried out to prevent the crop losses worldwide, every year. Therefore, understanding the molecular mechanisms of pathogenicity and plant resistance against pathogen is important. The resistance against pathogens is regulated by three important phytohormones viz. salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). Here we review possible role of CRISPR technology to understand the plant pathogenicity by mutating genes responsible for pathogen invasion or up-regulating the phytohormones genes or resistant genes. Thus hormone biosynthesis genes, receptor and feeding genes of pathogens could be important targets for modifications using CRISPR/Cas9 following multiplexing tool box strategy in order to edit multiple genes simultaneously to produce super plants. Here we put forward our idea thatthe genes would be either mutated in case of plant receptor protein targets of pathogens or up-regulation of resistant genes or hormone biosynthesis genes will be better choice for resistance against pathogens.

Flower-specific jasmonate signaling regulates constitutive floral defenses in wild tobacco.

Optimal defense (OD) theory predicts that within a plant, tissues are defended in proportion to their fitness value and risk of predation. The fitness value of leaves varies greatly and leaves are protected by jasmonate (JA)-inducible defenses. Flowers are vehicles of Darwinian fitness in flowering plants and are attacked by herbivores and pathogens, but how they are defended is rarely investigated. We used Nicotiana attenuata, an ecological model plant with well-characterized herbivore interactions to characterize defense responses in flowers. Early floral stages constitutively accumulate greater amounts of two well-characterized defensive compounds, the volatile (E)-α-bergamotene and trypsin proteinase inhibitors (TPIs), which are also found in herbivore-induced leaves. Plants rendered deficient in JA biosynthesis or perception by RNA interference had significantly attenuated floral accumulations of defensive compounds known to be regulated by JA in leaves. By RNA-seq, we found a JAZ gene, NaJAZi, specifically expressed in early-stage floral tissues. Gene silencing revealed that NaJAZi functions as a flower-specific jasmonate repressor that regulates JAs, (E)-α-bergamotene, TPIs, and a defensin. Flowers silenced in NaJAZi are more resistant to tobacco budworm attack, a florivore. When the defensin was ectopically expressed in leaves, performance of Manduca sexta larvae, a folivore, decreased. NaJAZi physically interacts with a newly identified NINJA-like protein, but not the canonical NINJA. This NINJA-like recruits the corepressor TOPLESS that contributes to the suppressive function of NaJAZi on floral defenses. This study uncovers the defensive function of JA signaling in flowers, which includes components that tailor JA signaling to provide flower-specific defense.

The highly buffered Arabidopsis immune signaling network conceals the functions of its components.

Plant immunity protects plants from numerous potentially pathogenic microbes. The biological network that controls plant inducible immunity must function effectively even when network components are targeted and disabled by pathogen effectors. Network buffering could confer this resilience by allowing different parts of the network to compensate for loss of one another's functions. Networks rich in buffering rely on interactions within the network, but these mechanisms are difficult to study by simple genetic means. Through a network reconstitution strategy, in which we disassemble and stepwise reassemble the plant immune network that mediates Pattern-Triggered-Immunity, we have resolved systems-level regulatory mechanisms underlying the Arabidopsis transcriptome response to the immune stimulant flagellin-22 (flg22). These mechanisms show widespread evidence of interactions among major sub-networks-we call these sectors-in the flg22-responsive transcriptome. Many of these interactions result in network buffering. Resolved regulatory mechanisms show unexpected patterns for how the jasmonate (JA), ethylene (ET), phytoalexin-deficient 4 (PAD4), and salicylate (SA) signaling sectors control the transcriptional response to flg22. We demonstrate that many of the regulatory mechanisms we resolved are not detectable by the traditional genetic approach of single-gene null-mutant analysis. Similar to potential pathogenic perturbations, null-mutant effects on immune signaling can be buffered by the network.

Induction of Jasmonic Acid-Associated Defenses by Thrips Alters Host Suitability for Conspecifics and Correlates with Increased Trichome Densities in Tomato.

Plant defenses inducible by herbivorous arthropods can determine performance of subsequent feeding herbivores. We investigated how infestation of tomato (Solanum lycopersicum) plants with the Western flower thrips (Frankliniella occidentalis) alters host plant suitability and foraging decisions of their conspecifics. We explored the role of delayed-induced jasmonic acid (JA)-mediated plant defense responses in thrips preference by using the tomato mutant def-1, impaired in JA biosynthesis. In particular, we investigated the effect of thrips infestation on trichome-associated tomato defenses. The results showed that when offered a choice, thrips preferred non-infested plants over infested wild-type plants, while no differences were observed in def-1. Exogenous application of methyl jasmonate restored the repellency effect in def-1. Gene expression analysis showed induction of the JA defense signaling pathway in wild-type plants, while activating the ethylene signaling pathway in both genotypes. Activation of JA defenses led to increases in type-VI leaf glandular trichome densities in the wild type, augmenting the production of trichome-associated volatiles, i.e. terpenes. Our study revealed that plant-mediated intraspecific interactions between thrips are determined by JA-mediated defenses in tomato. We report that insects can alter not only trichome densities but also the allelochemicals produced therein, and that this response might depend on the magnitude and/or type of the induction.

Transcriptomic characterization of gall tissue of Japanese elm tree (Ulmus davidiana var. japonica) induced by the aphid Tetraneura nigriabdominalis.

Insect galls are abnormal plant tissues induced by parasitic insect(s) for use as their habitat. In previous work, we suggested that gall tissues induced by the aphid Tetraneura nigriabdominalis on Japanese elm trees are less responsive than leaf tissues to jasmonic acid (JA), which is involved in the production of volatile organic compounds as a typical defensive reaction of plants against attack by insect pests. A comprehensive analysis of gene expression by RNA sequencing indicated that the number of JA responsive genes was markedly lower in gall tissues than in leaf tissues. This suggests that gall tissues are mostly defective in JA signaling, although JA signaling is not entirely compromised in gall tissue. Gene ontology analysis sheds light on some stress-related unigenes with higher expression levels in gall tissues, suggesting that host plants sense aphids as a biotic stress but are defective in the JA-mediated defense response in gall tissues.

The N-end rule pathway regulates pathogen responses in plants.

To efficiently counteract pathogens, plants rely on a complex set of immune responses that are tightly regulated to allow the timely activation, appropriate duration and adequate amplitude of defense programs. The coordination of the plant immune response is known to require the activity of the ubiquitin/proteasome system, which controls the stability of proteins in eukaryotes. Here, we demonstrate that the N-end rule pathway, a subset of the ubiquitin/proteasome system, regulates the defense against a wide range of bacterial and fungal pathogens in the model plant Arabidopsis thaliana. We show that this pathway positively regulates the biosynthesis of plant-defense metabolites such as glucosinolates, as well as the biosynthesis and response to the phytohormone jasmonic acid, which plays a key role in plant immunity. Our results also suggest that the arginylation branch of the N-end rule pathway regulates the timing and amplitude of the defense program against the model pathogen Pseudomonas syringae AvrRpm1.

Simultaneous induction of jasmonic acid and disease-responsive genes signifies tolerance of American elm to Dutch elm disease.

Dutch elm disease (DED), caused by three fungal species in the genus Ophiostoma, is the most devastating disease of both native European and North American elm trees. Although many tolerant cultivars have been identified and released, the tolerance mechanisms are not well understood and true resistance has not yet been achieved. Here we show that the expression of disease-responsive genes in reactions leading to tolerance or susceptibility is significantly differentiated within the first 144 hours post-inoculation (hpi). Analysis of the levels of endogenous plant defense molecules such as jasmonic acid (JA) and salicylic acid (SA) in tolerant and susceptible American elm saplings suggested SA and methyl-jasmonate as potential defense response elicitors, which was further confirmed by field observations. However, the tolerant phenotype can be best characterized by a concurrent induction of JA and disease-responsive genes at 96 hpi. Molecular investigations indicated that the expression of fungal genes (i.e. cerato ulmin) was also modulated by endogenous SA and JA and this response was unique among aggressive and non-aggressive fungal strains. The present study not only provides better understanding of tolerance mechanisms to DED, but also represents a first, verified template for examining simultaneous transcriptomic changes during American elm-fungus interactions.