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Results for “Plant Immunity”
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The bZIP54 (GBF2)-SARD1 module regulates salicylic acid-mediated resistance to Pst DC3000 in Arabidopsis.
Salicylic acid (SA)-mediated defense responses are crucial for plant immunity, yet transcription factors (TFs) that coordinate SA biosynthesis with immune activation remain incompletely characterized. Here, a basic leucine zipper (bZIP) TF, bZIP54, was identified as a positive regulator in response to Pseudomonas syringae pv. tomato (Pst) DC3000. Consistent with this finding, bZIP54 regulated SA accumulation and a suite of SA-related defense genes following Pst DC3000 infection. Mechanistically, bZIP54 directly bound to a G-box-like motif in the SARD1 promoter, activating its expression-an interaction that was further enhanced by SA. Genetic analysis demonstrated that SARD1 operates downstream of bZIP54 to confer resistance to Pst DC3000. Additionally, bZIP54 also contributed to defense against the fungal pathogen Sclerotinia sclerotiorum, indicating a broader role in plant immunity. Together, these findings revealed a bZIP54-SARD1 regulatory module, thus providing insights into the transcriptional networks governing disease resistance in Arabidopsis.
[Towards the general theory of immunity].
The molecular studies of plant immunity resulted in revealing general pattern in the mechanisms of innate resistance of plants, invertebrates and vertebrates. These studies removed an ambiguity in the estimate of the role of different immunomodulators (supressors, specific and non-specific elicitors) of plant parasites, and allowed approaching the general theory of immunity. Such theory could be based on guard model of Biezen and Jones (1999), according to which the specific elicitors of parasites work as a factor of pathogens. Their ability to suppress the immune response to infection is determined by bounding of signal proteins of plants and stopping the transmission of signal to the factors that regulate transcription. Resistance proteins recognize the complex and interacting with it turn the cellular metabolism to the induction of defense response.
Molecular chaperone Hsp90 associates with resistance protein N and its signaling proteins SGT1 and Rar1 to modulate an innate immune response in plants.
SGT1 and Rar1 are important signaling components of resistance (R) gene-mediated plant innate immune responses. Here we report that SGT1 and Rar1 associate with the molecular chaperone Hsp90. In addition, we show that Hsp90 associates with the resistance protein N that confers resistance to tobacco mosaic virus. This suggests that Hsp90-SGT1-Rar1 and R proteins might exist in one complex. Suppression of Hsp90 in Nicotiana benthamiana plants shows that it plays an important role in plant growth and development. In addition, Hsp90 suppression in NN plants compromises N-mediated resistance to tobacco mosaic virus. Our results reveal a new role for SGT1- and Rar1-associated chaperone machinery in R gene-mediated defense signaling.
Innate immunity in plants and animals: emerging parallels between the recognition of general elicitors and pathogen-associated molecular patterns.
Recent findings have highlighted remarkable similarities in the innate pathogen defense systems of plants, animals and insects. Pathogen-associated molecular patterns (PAMP) that are similar to those activating innate immune responses in animals have been shown to mediate the activation of plant defense. Moreover, recognition complexes that are structurally related to animal PAMP receptors are now being discovered in plants, suggesting a common evolutionary origin of pathogen defense systems in higher eukaryotes.
Innate immunity: from plants to humans.
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Pathogen-induced, NADPH oxidase-derived reactive oxygen intermediates suppress spread of cell death in Arabidopsis thaliana.
Plant immune responses are usually accompanied by the production of extracellular superoxide at and surrounding infection sites. Extracellular reactive oxygen intermediates (ROIs) in plants were proposed to drive programmed cell death correlated with disease resistance (the hypersensitive response). ROIs derived from this oxidative burst are generated by plasma membrane NADPH oxidases, anchored by gp91(phox) proteins related to those responsible for the respiratory oxidative burst activated in mammalian neutrophils during infection. Mutation of Arabidopsis thaliana respiratory burst oxidase (Atrboh) genes eliminated pathogen-induced ROI production but had only a modest effect on the hypersensitive response. We show that Atrboh function can be activated by exogenous ROIs. Unexpectedly, the subsequent oxidative burst can suppress cell death in cells surrounding sites of NADPH oxidase activation. This cell death requires salicylic acid, a plant immune system activator. Thus, ROIs generated by Atrboh proteins can antagonize salicylic acid-dependent pro-death signals. These results have implications for understanding how salicylic acid activates defense signaling in cells spatially removed from infection sites without causing cell death.
Antigens produced in plants by infection with chimeric plant viruses immunize against rabies virus and HIV-1.
The coat protein (CP) of alfalfa mosaic virus was used as a carrier molecule to express antigenic peptides from rabies virus and HIV. The antigens were separately cloned into the reading frame of alfalfa mosaic virus CP and placed under the control of the subgenomic promoter of tobacco mosaic virus CP in the 30BRz vector. The in vitro transcripts of recombinant virus with sequences encoding the antigenic peptides were synthesized from DNA constructs and used to inoculate tobacco plants. The plant-produced protein (virus particles) was purified and used for immunization of mice. Both antigens elicited specific virus-neutralizing antibodies in immunized mice.
Hydrogen peroxide induces a rapid production of nitric oxide in mung bean (Phaseolus aureus).
Nitric oxide (NO) has recently been identified as an important signaling molecule in plant immune response. The present study aims to investigate the signaling pathway that leads to NO production. Using the NO specific fluorescent dye DAF-2DA, we observed rapid production of NO in mung bean leaves after the addition of 10 mM hydrogen peroxide (H(2)O(2)). NO was probably produced by a NOS-like enzyme in plants, as the NO production was inhibited by l-NAME, a NOS inhibitor. The NOS-like activity in the total leaf protein preparation of mung bean (Phaseolus aureus) was elevated 8.3-fold after 10 mM H(2)O(2) treatment, as demonstrated using the chemiluminescence NOS assay. The NOS-like activity was BH(4) dependent: omitting BH(4) in the reaction mixture of NOS assay reduced the NOS activity by 76%. We also found that the H(2)O(2) induced NO production was mediated via calcium ion flux, as it was blocked in the presence of a calcium ion channel blocker, verapamil. Results from the present study identified H(2)O(2) as an upstream signal that leads to NO production in plants. H(2)O(2) and NO, besides acting as two independent signaling molecules in plant immune response, may interrelate to form an oxidative cell death (OCD) cycle.
A natural immunity-activating plant lectin, Viscum album agglutinin-I, induces apoptosis in human lymphocytes, monocytes, monocytic THP-1 cells and murine thymocytes.
A galactoside-specific plant lectin, Viscum album agglutinin-I (VAA-I) with protein synthesis-inhibiting properties, has been shown to be cytotoxic in various eukaryotic cells, in vitro above a 10 ng/ml concentration. Noncytotoxic concentrations of VAA-I induced mRNA expression and enhanced secretion of proinflammatory cytokines in cultures of human peripheral blood mononuclear cells. In an animal model VAA-I has been shown to stimulate natural killer cells and granulocytes. In this study, human peripheral blood lymphocytes (PBL), human peripheral blood monocytes (PBM), murine thymocytes and human monocytic THP-1 cells were incubated for 24 h in the presence of various concentrations of VAA-I. The apoptotic effect of VAA-I was analyzed by flow cytometry following staining of the apoptotic nuclei in the cells with PI in hypotonic buffer and quantitative detection of DNA breaks were analyzed by the terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling (TUNEL) assay. In cultures of all types of investigated cells, a dose-dependent VAA-I concentrations above 10 ng/ml in PBL and at 1 ng/ml VAA-I concentration in PBM, thymocytes and THP-1 cells, a lectin-induced increase of the apoptotic nuclei was observed. In 24-hour cultures of PBL and thymocytes, the ratios between apoptotic and nonapoptotic cells were enhanced 10 times and 8 times, respectively, by 100 ng/ml VAA-I compared to the negative control. The concentration of 100 micrograms/ml VAA-I only caused necrosis. The isolated A chain of the VAA-I induced apoptosis in PBL and thymocytes. In the culture of PBL the isolated B chain of the VAA-I was not effective indicating that cytokine induction by VAA-I is probably not involved in its apoptotic effect. On CD4+8+ thymocytes, VAA-I resulted in a reduced expression of CD8+ molecules that could be related to a loss of volume and increase of density, both characteristic features of apoptosis.
Microbial partnerships and molecular mechanisms in plant stress physiology for climate-resilient and sustainable farming.
Plant-microbial partnerships and their underlying molecular mechanisms are indispensable, natural drivers of improved nutrient acquisition and stress tolerance in the face of climate-driven environmental challenges. Modern multi-omics tools, when coupled with artificial intelligence and synthetic biology, enable the precise design of targeted bioinoculants and synthetic microbial consortia. Translating these advanced microbiome-based strategies into scalable, field-level agricultural applications provides a sustainable path toward securing global food production while maintaining soil health. Global climate change imposes multifaceted abiotic and biotic stresses on crops, disrupting physiological and molecular processes and threatening agricultural productivity. Plant-associated microbes represent an underexplored yet powerful ally in enhancing crop resilience. This review presents current knowledge of plant-microbe interactions and the molecular mechanisms governing plant stress physiology, with an emphasis on climate-resilient and sustainable farming. Hence, ever-changing environmental cues pose a significant burden on agricultural productivity, and plant-associated microbial communities modulate a cascade of physiological and molecular responses, including production of phytohormones, signaling, regulation of reactive oxygen species homeostasis, and activation of plant immune responses to help plants withstand stress and enhance productivity. Moreover, root exudates, phytohormones, and quorum sensing mediate the central communication networks, facilitating plant-microbe cross talk. Additionally, the advances in OMICs approaches aid in disentangling the molecular underpinnings of these interactions by providing mechanistic insights and potential candidate gene targets for crop improvement and stress resilience. In the post-genomic era, integrating artificial intelligence and big data analysis to optimize microbiome-based strategies for sustainable agriculture is a new frontier for disentangling plant-microbe symbiosis to improve soil health, enhance crop yields, and improve stress tolerance. Thus, by integrating the ecological, physiological, and molecular perspectives, this review highlights the transformative potential of harnessing plant-microbe symbiosis for climate-resilient and sustainable agriculture.
Signal recognition and transduction mediated by the tomato Pto kinase: a paradigm of innate immunity in plants.
Plant disease resistance is the result of an innate host defense mechanism, which relies on the ability of the plant to recognize pathogen invasion and to efficiently mount defense responses. In tomato, resistance to the pathogen Pseudomonas syringae is mediated by the specific interaction between the plant serine/threonine kinase Pto and the bacterial protein AvrPto. This article reviews molecular and biochemical properties that confer to Pto the capability to function as an intracellular receptor and to activate a signaling cascade leading to the induction of defense responses.
Induced Immunity in Plants.
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[Oxidation system and its role in immunity in plants].
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Inductive immunity of plants against parasitic fungi.
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Integrated Functional Characterization of Hemileia vastatrix Effector Candidates Reveals Coordinated Immune Suppression, Sequential Deployment and Compartment-Specific Targeting.
Coffee leaf rust, caused by the obligate biotrophic fungus Hemileia vastatrix, remains the most destructive disease of coffee worldwide. Although genomic and transcriptomic studies have identified a large number of candidate effectors, experimental evidence supporting their biological roles during infection remains limited. Here, we integrated functional assays, temporal expression profiling during coffee infection and subcellular localization analyses to investigate the biological properties of 44 H. vastatrix effector candidates (HvECs). Using the Pseudomonas fluorescens EtHAn effector delivery system in Nicotiana benthamiana, 15 HvECs consistently suppressed pattern-triggered immunity (PTI), indicating that immune suppression is a widespread property among the H. vastatrix effector repertoire, as assessed in this heterologous system. Five HvECs also attenuated AvrB-triggered effector-triggered immunity (ETI), and three suppressed both PTI and ETI, suggesting that a subset of HvECs targets conserved regulatory nodes shared by these interconnected immune pathways. Temporal expression profiling revealed sequential deployment of HvECs throughout infection, with distinct subsets predominating during pre-biotrophic development, host penetration or biotrophic colonization, consistent with stage-specific functions during fungal pathogenesis. Subcellular localization analyses further showed that HvECs preferentially accumulated in the nucleus or chloroplasts, compartments known as central hubs of plant immune regulation. This study provides the most comprehensive functional characterization of H. vastatrix effector candidates to date, establishes a biologically informed framework for prioritizing candidates for future identification of avirulence determinants recognized by SH resistance genes, and advances our understanding of how the coffee rust fungus orchestrates immune suppression across time and cellular space during pathogenesis.
Two pathways act in an additive rather than obligatorily synergistic fashion to induce systemic acquired resistance and PR gene expression.
BACKGROUND: Local infection with necrotizing pathogens induces whole plant immunity to secondary challenge. Pathogenesis-related genes are induced in parallel with this systemic acquired resistance response and thought to be co-regulated. The hypothesis of co-regulation has been challenged by induction of Arabidopsis PR-1 but not systemic acquired resistance in npr1 mutant plants responding to Pseudomonas syringae carrying the avirulence gene avrRpt2. However, experiments with ndr1 mutant plants have revealed major differences between avirulence genes. The ndr1-1 mutation prevents hypersensitive cell death, systemic acquired resistance and PR-1 induction elicited by bacteria carrying avrRpt2. This mutation does not prevent these responses to bacteria carrying avrB. RESULTS: Systemic acquired resistance, PR-1 induction and PR-5 induction were assessed in comparisons of npr1-2 and ndr1-1 mutant plants, double mutant plants, and wild-type plants. Systemic acquired resistance was displayed by all four plant lines in response to Pseudomonas syringae bacteria carrying avrB. PR-1 induction was partially impaired by either single mutation in response to either bacterial strain, but only fully impaired in the double mutant in response to avrRpt2. PR-5 induction was not fully impaired in any of the mutants in response to either avirulence gene. CONCLUSION: Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5. One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death. The other pathway is dependent on salicylic acid accumulation and acts through NPR1. At least two other pathways also contribute additively to PR-5 induction.
Cloning and expression analysis of cDNAs corresponding to genes activated in cucumber showing systemic acquired resistance after BTH treatment.
BACKGROUND: Infection of plants by necrotizing pathogens can lead to the rapid and localized induction of a complex set of defense responses resulting in a restriction of pathogen growth and spread. Subsequently, an increase of plant resistance against a broad spectrum of pathogens is observed systemically. This plant immunity is known as Systemic Acquired Resistance. To identify components of the transduction pathway, we cloned and analysed the expression pattern of several mRNAs accumulating in cucumber plants after induction of Systemic Acquired Resistance. RESULTS: We tested on cucumber different compounds known to induce systemic acquired resistance. Among these, BTH (benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester) proved to be very effective. mRNA RT-PCR differential display was used to identify mRNA sequences induced 24 hours after the application of 10 microM BTH to cucumber plants. A cDNA library constructed from cucumber plants sprayed with 10 microM BTH was screened to get corresponding full length cDNAs. Among the identified cDNAs were those coding for a putative ras-related GTP-binding protein, a putative beta-1,4-N-Acetylglucosaminyltranferase III and a putative pathogenesis related protein. The time course of accumulation of the three corresponding mRNAs was analysed by northern blotting in plants treated by BTH or in plants infected by Colletotrichum lagenarium. CONCLUSIONS: The mRNA RT-PCR differential display technique allowed the identification of three genes possibly involved in Systemic Acquired Resistance in cucumber. Pathogenesis-related proteins are known to be involved in plant defence against pathogens. GTP-binding protein and N-acetylglucosaminyltranferase III have been reported to be components of signal transduction pathways in mammals and plants.