Activation Of Defense Responses Research Articles

Wheat TaNACα18 functions as a positive regulator of high-temperature adaptive responses and improves cell defense machinery.

Global wheat production amounted to >780 MMT during 2022-2023 whose market size are valued at >$128 billion. Wheat is highly susceptible to high-temperature stress (HTS) throughout the life cycle and its yield declines 5-7% with the rise in each degree of temperature. Previously, we reported an array of HTS-response markers from a resilient wheat cv. Unnat Halna and described their putative role in heat acclimation. To complement our previous results and identify the key determinants of thermotolerance, here we examined the cytoplasmic proteome of a sensitive cv. PBW343. The HTS-triggered metabolite reprograming highlighted how proteostasis defects influence the formation of an integrated stress-adaptive response. The proteomic analysis identified several promising HTS-responsive proteins, including a NACα18 protein, designated TaNACα18, whose role in thermotolerance remains unknown. Dual localization of TaNACα18 suggests its crucial functions in the cytoplasm and nucleus. The homodimerization of TaNACα18 anticipated its function as a transcriptional coactivator. The complementation of TaNACα18 in yeast and overexpression in wheat demonstrated its role in thermotolerance across the kingdom. Altogether, our results suggest that TaNACα18 imparts tolerance through tight regulation of gene expression, cell wall remodeling and activation of cell defense responses.

Roles of microbiota in autoimmunity in Arabidopsis leaves

Over the past three decades, researchers have isolated plant mutants that show constitutively activated defence responses in the absence of pathogen infection. These mutants are called autoimmune mutants and are typically dwarf and/or bearing chlorotic/necrotic lesions. Here, from a genetic screen for Arabidopsis genes involved in maintaining a normal leaf microbiota, we identified TIP GROWTH DEFECTIVE 1 (TIP1), which encodes an S-acyltransferase, as a key player in guarding leaves against abnormal microbiota level and composition under high-humidity conditions. The tip1 mutant has several characteristic phenotypes of classical autoimmune mutants, including a dwarf stature, showing lesions, and having a high basal level of defence gene expression. Gnotobiotic experiments revealed that the autoimmune phenotypes of the tip1 mutant are largely dependent on the presence of microbiota as axenic tip1 plants have markedly reduced autoimmune phenotypes. We found that the microbiota dependency of autoimmune phenotypes is shared by several ‘lesion mimic’-type autoimmune mutants in Arabidopsis. It is worth noting that autoimmune phenotypes caused by mutations in two Nucleotide-Binding, Leucine-Rich Repeat (NLR) genes do not require the presence of microbiota and can even be partially alleviated by microbiota. Our results therefore suggest the existence of at least two classes of autoimmunity (microbiota-dependent versus microbiota-independent) in plants. The observed interplay between autoimmunity and microbiota in the lesion mimic class of autoimmunity is reminiscent of the interactions between autoimmunity and dysbiosis in the animal kingdom. These parallels highlight the intricate relationship between host immunity and microbial communities across various biological systems.

Alternaria solani core effector Aex59 is a new member of the Alt a 1 protein family and is recognized as a PAMP

Early blight caused by Alternaria solani is a destructive disease in potato production. Here, through systematically screening of an effector protein pool consisting of 115 small cysteine-containing candidate Aex (Alternariaextracellular proteins) in A. solani, we identified a core effector protein named Aex59, a pathogen-associated molecular pattern (PAMP) molecule. Aex59 is uniquely present in the Ascomycota of fungi and can activate defense responses in multiple plants. Targeted gene disruption showed that Aex59 is a virulence factor and participates in spore development. Perception of Aex59 in Nicotiana benthamiana does not depend on the receptor-like kinases Brassinosteroid-associated kinase1 (BAK1) and Suppressor of BIR1-1 (SOBIR1), which are required for multiple pattern recognition receptors (PRR) pathways. Sequence analysis revealed that Aex59 is a new member of the Alt a 1 protein family and is a potential molecular marker capable of aiding in the classification of the fungi Alternaria spp.

A delayed response in phytohormone signaling and production contributes to pine susceptibility to Fusarium circinatum

BackgroundFusarium circinatum is the causal agent of pine pitch canker disease, which affects Pinus species worldwide, causing significant economic and ecological losses. In Spain, two Pinus species are most affected by the pathogen; Pinus radiata is highly susceptible, while Pinus pinaster has shown moderate resistance. In F. circinatum-Pinus interactions, phytohormones are known to play a crucial role in plant defense. By comparing species with different degrees of susceptibility, we aimed to elucidate the fundamental mechanisms underlying resistance to the pathogen. For this purpose, we used an integrative approach by combining gene expression and metabolomic phytohormone analyses at 5 and 10 days post inoculation.ResultsGene expression and metabolite phytohormone contents suggested that the moderate resistance of P. pinaster to F. circinatum is determined by the induction of phytohormone signaling and hormone rearrangement beginning at 5 dpi, when symptoms are still not visible. Jasmonic acid was the hormone that showed the greatest increase by 5 dpi, together with the active gibberellic acid 4 and the cytokinin dehydrozeatin; there was also an increase in abscisic acid and salicylic acid by 10 dpi. In contrast, P. radiata hormonal changes were delayed until 10 dpi, when symptoms were already visible; however, this increase was not as high as that in P. pinaster. Indeed, in P. radiata, no differences in jasmonic acid or salicylic acid production were found. Gene expression analysis supported the hormonal data, since the activation of genes related to phytohormone synthesis was observed earlier in P. pinaster than in the susceptible P. radiata.ConclusionsWe determine that the moderate resistance of P. pinaster to F. circinatum is in part a result of early and strong activation of plant phytohormone-based defense responses before symptoms become visible. We suggest that jasmonic acid signaling and production are strongly associated with F. circinatum resistance. In contrast, P. radiata susceptibility was attributed to a delayed response to the fungus at the moment when symptoms were visible. Our results contribute to a better understanding of the phytohormone-based defense mechanism involved in the Pinus-F. circinatum interactions and provide insight into the development of new strategies for disease mitigation.

A conserved oomycete effector RxLR23 triggers plant defense responses by targeting ERD15La to release NbNAC68

Oomycete pathogens deliver many effectors to enhance virulence or suppress plant immunity. Plant immune networks are interconnected, in which a few effectors can trigger a strong defense response when recognized by immunity-related proteins. How effectors activate plant defense response remains poorly understood. Here we report Phytophthora capsici effector RxLR23KM can induce plant cell death and plant immunity. RxLR23KM specifically binds to ERD15La, a regulator of abscisic acid and salicylic acid pathway, and the binding intensity depends on the amino acid residues (K93 and M320). NbNAC68, a downstream protein of ERD15La, can stimulate plant immunity that is compromised after binding with ERD15La. Silencing of NbNAC68 substantially prevents the activation of plant defense response. RxLR23KM binds to ERD15La, releasing NbNAC68 to activate plant immunity. These findings highlight a strategy of plant defense response that ERD15La as a central regulator coordinates RxLR23KM to regulate NbNAC68-triggered plant immunity.

Unlocking the Transcriptional Reprogramming Repertoire between Variety-Dependent Responses of Grapevine Berries to Infection by Aspergillus carbonarius.

Aspergillus carbonarius causes severe decays on berries in vineyards and is among the main fungal species responsible for grape contamination by ochratoxin A (OTA), which is the foremost mycotoxin produced by this fungus. The main goal of this study was to investigate at the transcriptome level the comparative profiles between two table grape varieties (Victoria and Fraoula, the white and red variety, respectively) after their inoculation with a virulent OTA-producing A. carbonarius strain. The two varieties revealed quite different transcriptomic signatures and the expression profiles of the differential expressed genes (DEGs) highlighted distinct and variety-specific responses during the infection period. The significant enrichment of pathways related to the modulation of transcriptional dynamics towards the activation of defence responses, the triggering of the metabolic shunt for the biosynthesis of secondary metabolites, mainly phenylpropanoids, and the upregulation of DEGs encoding phytoalexins, transcription factors, and genes involved in plant-pathogen interaction and immune signaling transduction was revealed in an early time point in Fraoula, whereas, in Victoria, any transcriptional reprogramming was observed after a delay. However, both varieties, to some extent, also showed common expression dynamics for specific DEG families, such as those encoding for laccases and stilbene synthases. Jasmonate (JA) may play a critical modulator role in the defence machinery as various JA-biosynthetic DEGs were upregulated. Along with the broader modulation of the transcriptome that was observed in white grape, expression profiles of specific A. carbonarius genes related to pathogenesis, fungal sporulation, and conidiation highlight the higher susceptibility of Victoria. Furthermore, the A. carbonarius transcriptional patterns directly associated with the regulation of the pathogen OTA-biosynthesis gene cluster were more highly induced in Victoria than in Fraoula. The latter was less contaminated by OTA and showed substantially lower sporulation. These findings contribute to uncovering the interplay beyond this plant-microbe interaction.

SERKs serve as co-receptors for SYR1 to trigger systemin-mediated defense responses in tomato.

Systemin, the first peptide hormone identified in plants, was initially isolated from tomato (Solanum lycopersicum) leaves. Systemin mediates local and systemic wound-induced defense responses in plants, conferring resistance to necrotrophic fungi and herbivorous insects. Systemin is recognized by the leucine-rich-repeat receptor-like kinase (LRR-RLK) receptor SYSTEMIN RECEPTOR1 (SYR1), but how the systemin recognition signal is transduced to intracellular signaling pathways to trigger defense responses is poorly understood. Here, we demonstrate that SERK family LRR-RLKs function as co-receptors for SYR1 to mediate systemin signal transduction in tomato. By using chemical genetic approaches coupled with engineered receptors, we revealed that the association of the cytoplasmic kinase domains of SYR1 with SERKs leads to their mutual trans-phosphorylation and the activation of SYR1, which in turn induces a wide range of defense responses. Systemin stimulates the association between SYR1 and all tomato SERKs (SlSERK1, SlSERK3A, and SlSERK3B). The resulting SYR1-SlSERK heteromeric complexes trigger the phosphorylation of TOMATO PROTEIN KINASE 1B (TPK1b), a receptor-like cytoplasmic kinase that positively regulates systemin responses. Additionally, upon association with SYR1, SlSERKs are cleaved by the Pseudomonas syringae effector HopB1, further supporting the finding that SlSERKs are activated by systemin-bound SYR1. Finally, genetic analysis using Slserk mutants showed that SlSERKs are essential for systemin-mediated defense responses. Collectively, these findings demonstrate that the systemin-mediated association of SYR1 and SlSERKs activates defense responses against herbivorous insects.

An indole-3-acetic acid inhibitor mitigated mild cadmium stress by suppressing peroxide formation in rice seedling roots

Cadmium (Cd) is a widely distributed heavy metal pollutant that is detrimental to growth and development of plants. The secretion of indole-3-acetic acid is one of the defense mechanisms when plants inflict heavy metal stress. This study aimed to explore how 4-phenoxyphenylboronic acid, an effective IAA inhibitor, induces changes in IAA level, Cadmium accumulation, and activation of defense responses in rice seedling roots under different Cadmium concentrations. Our research results show that: 1) root growth was promoted with PPBa addition under mild Cadmium treatment. 2) the root IAA level improved with increasing Cadmium concentration, and PPBa had a significant inhibitory effect on IAA level. 3) PPBa had no effect on the Cadmium accumulation in rice seedling roots. 4) PPBa had a significant inhibitory effect on the generation of H2O2 under mild and moderate Cadmium treatment. 5) PPBa exacerbated the imbalance of osmotic substances in rice seedling roots under severe Cadmium treatment. This study helps us understand the tolerance and endogenous regulation of plants to heavy metal stress.

Myosin XI-mediated BIK1 recruitment to nanodomains facilitates FLS2–BIK1 complex formation during innate immunity in Arabidopsis

Plants rely on immune receptor complexes at the cell surface to perceive microbial molecules and transduce these signals into the cell to regulate immunity. Various immune receptors and associated proteins are often dynamically distributed in specific nanodomains on the plasma membrane (PM). However, the exact molecular mechanism and functional relevance of this nanodomain targeting in plant immunity regulation remain largely unknown. By utilizing high spatiotemporal resolution imaging and single-particle tracking analysis, we show that myosin XIK interacts with remorin to recruit and stabilize PM-associated kinase BOTRYTIS-INDUCED KINASE 1 (BIK1) within immune receptor FLAGELLIN SENSING 2 (FLS2)-containing nanodomains. This recruitment facilitates FLS2/BIK1 complex formation, leading to the full activation of BIK1-dependent defense responses upon ligand perception. Collectively, our findings provide compelling evidence that myosin XI functions as a molecular scaffold to enable a spatially confined complex assembly within nanodomains. This ensures the presence of a sufficient quantity of preformed immune receptor complex for efficient signaling transduction from the cell surface.

Transcriptome analysis of Phytophthora cactorum infecting strawberry identified RXLR effectors that induce cell death when transiently expressed in Nicotiana benthamiana

Phytophthora cactorum is a plant pathogenic oomycete that causes crown rot in strawberry leading to significant economic losses every year. To invade the host, P. cactorum secretes an arsenal of effectors that can manipulate host physiology and impair its defense system promoting infection. A transcriptome analysis was conducted on a susceptible wild strawberry genotype (Fragaria vesca) 48 hours post inoculation with P. cactorum to identify effectors expressed during the early infection stage. The analysis revealed 4,668 P. cactorum genes expressed during infection of F. vesca. A total of 539 secreted proteins encoded by transcripts were identified, including 120 carbohydrate-active enzymes, 40 RXLRs, 23 proteolytic enzymes, nine elicitins, seven cysteine rich proteins, seven necrosis inducing proteins and 216 hypothetical proteins with unknown function. Twenty of the 40 RXLR effector candidates were transiently expressed in Nicotiana benthamiana using agroinfiltration and five previously unreported RXLR effector genes (Pc741, Pc8318, Pc10890, Pc20813, and Pc22290) triggered cell death when transiently expressed. The identified cell death inducing RXLR effectors showed 31–66% identity to known RXLR effectors in different Phytophthora species having roles in pathogenicity including both activation and suppression of defense response in the host. Furthermore, homology analysis revealed that these cell death inducing RXLR effectors were highly conserved (82 - 100% identity) across 23 different strains of P. cactorum originating from apple or strawberry.

GLR-dependent calcium and electrical signals are not coupled to systemic, oxylipin-based wound-induced gene expression in Marchantia polymorpha.

In angiosperms, wound-derived signals travel through the vasculature to systemically activate defence responses throughout the plant. In Arabidopsis thaliana, activity of vasculature-specific Clade 3 glutamate receptor-like (GLR) channels is required for the transmission of electrical signals and cytosolic Ca2+ ([Ca2+]cyt) waves from wounded leaves to distal tissues, triggering activation of oxylipin-dependent defences. Whether nonvascular plants mount systemic responses upon wounding remains unknown. To explore the evolution of systemic defence responses, we investigated electrical and calcium signalling in the nonvascular plant Marchantia polymorpha. We found that electrical signals and [Ca2+]cyt waves are generated in response to mechanical wounding and propagated to nondamaged distal tissues in M. polymorpha. Functional analysis of MpGLR, the only GLR encoded in the genome of M. polymorpha, indicates that its activity is necessary for the systemic transmission of wound-induced electrical signals and [Ca2+]cyt waves, similar to vascular plants. However, spread of these signals is neither coupled to systemic accumulation of oxylipins nor to a transcriptional defence response in the distal tissues of wounded M. polymorpha plants. Our results suggest that lack of vasculature prevents translocation of additional signalling factors that, together with electrical signals and [Ca2+]cyt waves, contribute to systemic activation of defences in tracheophytes.

Modulation of plant immunity and biotic interactions under phosphate deficiency.

Phosphorus (P) is an essential macronutrient for plant life and growth. P is primarily acquired in the form of inorganic phosphate (Pi) from soil. To cope with Pi deficiency, plants have evolved an elaborate system to improve Pi acquisition and utilization through an array of developmental and physiological changes, termed Pi starvation response (PSR). Plants also assemble and manage mutualistic microbes to enhance Pi uptake, through integrating PSR and immunity signaling. A trade-off between plant growth and defense favors the notion that plants lower a cellular state of immunity to accommodate host-beneficial microbes for nutrition and growth at the cost of infection risk. However, the existing data indicate that plants selectively activate defense responses against pathogens, but do not or less against non-pathogens, even under nutrient deficiency. In this review, we highlight recent advances in the principles and mechanisms with which plants balance immunity and growth-related processes to optimize their adaptation to Pi deficiency.

Phylogenetic Analysis of Wall-Associated Kinase Genes in Triticum Species and Characterization of TaWAK7 Involved in Wheat Powdery Mildew Resistance.

Wall-associated kinases (WAKs), a group of receptor-like kinases, have been found to play important roles in defending against pathogens and in various developmental processes. However, the importance of this family in wheat remains largely unknown. Wheat powdery mildew is caused by Blumeria graminis f. sp. tritici (Bgt), which initiates infection on the cell surface and forms haustoria inside the cell; therefore, the defense to Bgt involves extracellular and subsequently intracellular signals. In this study, WAKs were identified genome-wide and analyzed phylogenetically, and then a transmembrane WAK gene that putatively participated in pathogen-associated molecular pattern-triggered immunity and effector-triggered immunity to Bgt was functionally and evolutionarily investigated. In total, 1,193 WAKs were identified from wheat and its Gramineae relatives. Phylogenetic analysis indicated that WAKs expanded through tandem duplication or segment duplication. TaWAK7, from chromosome 2A, was identified as a Bgt-inducible gene both in susceptible and resistant materials, but it showed distinct responsive patterns. Functional analysis showed that TaWAK7 was involved in both the basal and resistance gene-mediated resistances. The specific gene structures and protein characteristics of TaWAK7, along with its orthologs, were characterized both in subgenomes of Triticum spp. and in the A genome of multiple wheat accessions, which revealed that TaWAK7 orthologs underwent complex evolution with frequent gene fusion and domain deletion. In addition, three cytoplasmic proteins interacting with TaWAK7 were indicated by yeast two-hybrid and bimolecular fluorescence complementation assays. Binding of TaWAK7 with these proteins could change its subcellular localization from the plasma membrane to the cytoplasm. This study provides a better understanding of the evolution of WAKs at the genomic level and TaWAK7 at the gene level and provides useful clues for further investigation of how WAKs transmit the extracellular signals to the cytoplasm to activate defense responses.

Guardians of wheat: Unleashing transgenerational immune priming with Trichoderma against spot blotch

Plants encounter various biotic stresses in their natural habitat, prompting the exploration of innovative protective measures to bolster their immune defences against pathogens. An effective strategy involves priming plant immunity, conferring enduring and comprehensive protection. Defence priming, characterized by heightened responsiveness to attackers following prior stress exposure, intriguingly manifests transgenerationally, transmitting the memory of priming to subsequent plant generations. In our investigation, we delved into the phenomenon of transgenerational immune priming (TGIP) in wheat facilitated by Trichoderma, spanning from the parental generation (G0) to the grand progeny (G2) generation. Successful establishment of transgenerational priming in the G2 generation was achieved by initially priming the G0 generation of wheat with Trichoderma. To assess priming inheritance, seeds from the G1 generation were collected, and both primed and non-primed wheat plants' grand progeny (G2 generation) were cultivated in soil. Subsequent evaluation encompassed the disease phenotype, biochemical parameters, and yield-related traits of the G2 generation wheat when confronted with Bipolaris sorokiniana, the causal agent of spot blotch disease. Our analysis revealed that the G2 generation of primed wheat displayed superior protection against spot blotch compared to non-primed wheat. Biochemical studies indicated no activation of defensive responses in the absence of disease pressure in G2 wheat plants. However, upon pathogen challenge, the grand progeny of primed wheat exhibited a robust defence response, surpassing that of non-primed wheat. This targeted defence response enabled efficient resource utilization and mitigated yield penalties. Furthermore, under biotic stress conditions, the grand progeny of primed wheat exhibited enhanced yield parameters compared to non-primed wheat. Our findings provide conclusive evidence that Trichoderma-mediated priming against B. sorokiniana can be inherited successfully from the parental (G0) generation to the grand progeny (G2) generation of wheat. This study represents the initial documentation of Trichoderma-mediated TGIP in wheat against B. sorokiniana, holding significant promise for sustainable agriculture by offering an environmentally friendly alternative to chemical pesticides.

Knock-out of BnHva22c reduces the susceptibility of Brassica napus to infection with the fungal pathogen Verticillium longisporum

Verticillium longisporum (Vl43) is a soilborne hemibiotrophic fungal pathogen causing stem striping on oilseed rape (OSR) and severe yield losses. Breeding for resistant varieties is the most promising approach to control this disease. Here, we report the identification of Hva22c as a novel susceptibility factor and its potential for improving OSR resistance. Hva22c is a member of the Hva22 gene family, originally described for barley (Hordeum vulgare). Several Hva22 members have been located at the endoplasmic reticulum. Hva22c is up-regulated in response to Vl43 in both Arabidopsis and OSR. We demonstrate that knock-out of Hva22c in OSR by CRISPR/Cas9 and its homolog in Arabidopsis by T-DNA insertion reduced plants’ susceptibility toVl43infection and impaired the development of disease symptoms. To understand the underlying mechanism, we analysed transcriptomic data from infected and non-infected roots of hva22c knock-out and wild type plants. We identified a homozygous mutant with frame-shifts in all four BnHva22c loci displaying a vastly altered transcriptional landscape at 6 dpi. Significantly, a large set of genes was suppressed under mock conditions including genes related to the endomembrane systems. Among the up-regulated genes we found several defense-related and phytohormone-responsive genes when comparing mutant to the wild type. These results demonstrate that Hva22c is functionally required for a fully compatible plant-fungus interaction. Its loss of function reduces plant susceptibility, most likely due to endoplasmatic reticulum and Golgi dysfunction accompanied by additionally activated defense responses. These findings can help improve OSR resistance to V. longisporum infection.

Metabolomic insights into the browning inhibition of fresh-cut apple by hydrogen sulfide

Hydrogen sulfide (H2S) is known to effectively inhibit the browning of fresh-cut apples, but the mechanism at a metabolic level remains unclear. Herein, non-targeted metabolomics was used to analyze metabolic changes in surface and internal tissues of fresh-cut apple after H2S treatment. The results showed that prenol lipids were the most up-accumulated differential metabolites in both surface and inner tissue of fresh-cut apple during browning process, which significantly down-accumulated by H2S treatment. H2S treatment reduced the consumption of amino acid in surface tissue. Regarding inner tissue, H2S activated defense response through accumulation of lysophospholipid signaling and induced the biosynthesis of phenolic compounds. We therefore propose that H2S inhibited the surface browning of fresh-cut apple by reducing the accumulation of prenol lipids, directly delaying amino acid consumption in surface tissue and indirectly regulating defense response in inner tissue, which provides fundamental insights into browning inhibition mechanisms by H2S.

The Caenorhabditis elegans proteome response to two protective Pseudomonas symbionts.

The Caenorhabditis elegans natural microbiota isolates Pseudomonas lurida MYb11 and Pseudomonas fluorescens MYb115 protect the host against pathogens through distinct mechanisms. While P. lurida produces an antimicrobial compound and directly inhibits pathogen growth, P. fluorescens MYb115 protects the host without affecting pathogen growth. It is unknown how these two protective microbes affect host biological processes. We used a proteomics approach to elucidate the C. elegans response to MYb11 and MYb115. We found that both Pseudomonas isolates increase vitellogenin protein production in young adults, which confirms previous findings on the effect of microbiota on C. elegans reproductive timing. Moreover, the C. elegans responses to MYb11 and MYb115 exhibit common signatures with the response to other vitamin B12-producing bacteria, emphasizing the importance of vitamin B12 in C. elegans-microbe metabolic interactions. We further analyzed signatures in the C. elegans response specific to MYb11 or MYb115. We provide evidence for distinct modifications in lipid metabolism by both symbiotic microbes. We could identify the activation of host-pathogen defense responses as an MYb11-specific proteome signature and provide evidence that the intermediate filament protein IFB-2 is required for MYb115-mediated protection. These results indicate that MYb11 not only produces an antimicrobial compound but also activates host antimicrobial defenses, which together might increase resistance to infection. In contrast, MYb115 affects host processes such as lipid metabolism and cytoskeleton dynamics, which might increase host tolerance to infection. Overall, this study pinpoints proteins of interest that form the basis for additional exploration into the mechanisms underlying C. elegans microbiota-mediated protection from pathogen infection and other microbiota-mediated traits.IMPORTANCESymbiotic bacteria can defend their host against pathogen infection. While some protective symbionts directly interact with pathogenic bacteria, other protective symbionts elicit a response in the host that improves its own pathogen defenses. To better understand how a host responds to protective symbionts, we examined which host proteins are affected by two protective Pseudomonas bacteria in the model nematode Caenorhabditis elegans. We found that the C. elegans response to its protective symbionts is manifold, which was reflected in changes in proteins that are involved in metabolism, the immune system, and cell structure. This study provides a foundation for exploring the contribution of the host response to symbiont-mediated protection from pathogen infection.

Integrated transcriptome and DNA methylome analysis reveal the biological base of increased resistance to gray leaf spot and growth inhibition in interspecific grafted tomato scions.

Grafting is widely used as an important agronomic approach to deal with environmental stresses. However, the molecular mechanism of grafted tomato scions in response to biotic stress and growth regulation has yet to be fully understood. This study investigated the resistance and growth performance of tomato scions grafted onto various rootstocks. A scion from a gray leaf spot-susceptible tomato cultivar was grafted onto tomato, eggplant, and pepper rootstocks, creating three grafting combinations: one self-grafting of tomato/tomato (TT), and two interspecific graftings, namely tomato/eggplant (TE) and tomato/pepper (TP). The study utilized transcriptome and DNA methylome analyses to explore the regulatory mechanisms behind the resistance and growth traits in the interspecific graftings. Results indicated that interspecific grafting significantly enhanced resistance to gray leaf spot and improved fruit quality, though fruit yield was decreased compared to self-grafting. Transcriptome analysis demonstrated that, compared to self-grafting, interspecific graftings triggered stronger wounding response and endogenous immune pathways, while restricting genes related to cell cycle pathways, especially in the TP grafting. Methylome data revealed that the TP grafting had more hypermethylated regions at CHG (H = A, C, or T) and CHH sites than the TT grafting. Furthermore, the TP grafting exhibited increased methylation levels in cell cycle related genes, such as DNA primase and ligase, while several genes related to defense kinases showed decreased methylation levels. Notably, several kinase transcripts were also confirmed among the rootstock-specific mobile transcripts. The study concludes that interspecific grafting alters gene methylation patterns, thereby activating defense responses and inhibiting the cell cycle in tomato scions. This mechanism is crucial in enhancing resistance to gray leaf spot and reducing growth in grafted tomato scions. These findings offer new insights into the genetic and epigenetic contributions to agronomic trait improvements through interspecific grafting.

Global Transcriptome Analysis of the Peach (Prunus persica) in the Interaction System of Fruit-Chitosan-Monilinia fructicola.

The peach (Prunus persica L.) is one of the most important stone-fruit crops worldwide. Nevertheless, successful peach fruit production is seriously reduced by losses due to Monilinia fructicola the causal agent of brown rot. Chitosan has a broad spectrum of antimicrobial properties and may also act as an elicitor that activate defense responses in plants. As little is known about the elicitation potential of chitosan in peach fruits and its impact at their transcriptional-level profiles, the aim of this study was to uncover using RNA-seq the induced responses regulated by the action of chitosan in fruit-chitosan-M. fructicola interaction. Samples were obtained from fruits treated with chitosan or inoculated with M. fructicola, as well from fruits pre-treated with chitosan and thereafter inoculated with the fungus. Chitosan was found to delay the postharvest decay of fruits, and expression profiles showed that its defense-priming effects were mainly evident after the pathogen challenge, driven particularly by modulations of differentially expressed genes (DEGs) related to cell-wall modifications, pathogen perception, and signal transduction, preventing the spread of fungus. In contrast, as the compatible interaction of fruits with M. fructicola was challenged, a shift towards defense responses was triggered with a delay, which was insufficient to limit fungal expansion, whereas DEGs involved in particular processes have facilitated early pathogen colonization. Physiological indicators of peach fruits were also measured. Additionally, expression profiles of particular M. fructicola genes highlight the direct antimicrobial activity of chitosan against the fungus. Overall, the results clarify the possible mechanisms of chitosan-mediated tolerance to M. fructicola and set new foundations for the potential employment of chitosan in the control of brown rot in peaches.

Differential expression of antimicrobial metabolites, phenylpropanoid and phytohormone metabolic pathway genes determines resistance or susceptibility to Ascochyta rabiei in chickpea

AbstractBlight caused by Ascochyta rabiei is a major constraint in the productivity of chickpea (Cicer arietinum). The mechanisms governing resistance/susceptibility to blight in chickpea are poorly understood. We used a blight‐resistant (HC1) and a blight‐susceptible (GPF2) genotype of chickpea and genes of pathogenesis‐related proteins (PRPs), phenylpropanoid pathway metabolites, abscisic acid (ABA), gibberellic acid (GA) and jasmonic acid (JA) to understand the role of these in A. rabiei resistance/susceptibility. The JA, ABA and GA biosynthesis genes of chickpea were retrieved, characterized and gene‐specific primers were used for transcriptional studies. Gene expression revealed that chickpea activated its defences rather quickly and well before initiation of spore germination. In resistant HC1, the majority of the JA, GA and phenylpropanoid pathway genes had peak maxima at 2 h post‐inoculation (hpi) whereas PRPs/defence genes had peak maxima at 24/36 hpi implying that defence to A. rabiei in chickpea is composed of a two‐tier system separated by time: immediately after spore attachment and at or just prior to host penetration. Unlike HC1, susceptible GPF2 was late in activation of defence responses or did not activate them. Another striking difference between HC1 and GPF2 was up‐regulation of ABA biosynthesis genes in inoculated GPF2 and down‐regulation in HC1. This study revealed that phenylpropanoids, PRPs, JA, 8‐(1R,2R)‐3‐oxo‐2‐(Z)‐pent‐2‐enyl cyclopentyl octanoate, (15Z)‐12‐oxophyto‐10,15‐dienoic acid and methyl‐jasmonate govern resistance to A. rabiei in chickpea whereas ABA governs susceptibility.