Extracellular pyridine nucleotides mediate systemic acquired resistance in Arabidopsis thaliana
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE225107 | GEO | 2023/10/02
REPOSITORIES: GEO
Similar Datasets
Project description:N-hydroxy-pipecolic acid (NHP) is a mobile metabolite essential for inducing and amplifying systemic acquired resistance (SAR) following pathogen attack. In Arabidopsis thaliana (Arabidopsis), exogenous NHP is sufficient to activate SAR-related immune responses, including salicylic acid (SA) accumulation and changes in global transcriptional profile. Previous studies have tracked these changes 1-2 days after an initial NHP treatment, resulting in little knowledge of the very early phases of NHP signaling and transcriptional responses leading to immunity. Here we show NHP elicits transcriptional changes within minutes of treatment. We report distinct waves of expression over the course of minutes to hours defined by transient induction of jasmonic acid/wound-related responses, a primary induction of WRKY transcription factor expression, and subsequent induction of WRKY-regulated defense genes. The upregulation of WRKYs and the majority of defense-related genes occurred in the sid2-2 mutant, which is unable to accumulate SA upon NHP treatment, suggesting NHP is sufficient to drive the early phase of transcriptional changes in a low SA environment. We also show that WRKY70 is required for the expression of a set of genes defining the secondary transcriptional changes, as well as NHP enhancement of ROS production and SAR.
2024-08-16 | GSE263276 | GEO
Project description:The goal of the microarray was to compare the bacterial pathogen Pseudomonas syringae pv. maculicola ES4326 (Psm)-induced transcriptome changes in the systemic leaves of the wild-type Col-0, lecrk-VI.2-2, and bak1-5 plants. Results showed that local Psm inoculation induced dramatic transcriptional changes in Col-0, with 564 and 151 genes up- and down-regulated at least twofold with a low q value (≤ 0.05), respectively. However, only 55 and 26 genes in lecrk-VI.2-2 and 221 and 121 genes in bak1-5 were up- and down-regulated, respectively. The majority of the genes that were induced or suppressed twofold or more with a low q value (≤ 0.05) in Col-0 were induced or suppressed to a smaller extent in bak1-5 and the smallest extent in lecrk-VI.2-2. These results indicate that both lecrk-VI.2-2 and bak1-5 suppressed Psm-induced systemic signaling with the lecrk-VI.2-2 mutation having a stronger effect than bak1-5.
2019-10-29 | GSE121886 | GEO
Project description:After localized invasion by bacterial pathogens, systemic acquired resistance (SAR) is induced in uninfected plant tissues, resulting in enhanced defense against a broad range of pathogens. Although SAR requires mobilization of signaling molecules via the plant vasculature, the specific mechanisms remain elusive. The lipid transfer protein-defective in induced resistance 1-1 (DIR1-1) was identified in Arabidopsis thaliana by screening for mutants that were defective in SAR. Since then, the structure and lipid-binding properties of DIR1 have been determined, showing that its barrel structure can bind two, long-chain fatty-acid molecules. Several SAR mobile signals, including dehydroabietinal (DA), azelaic acid (AzA), and glycerol-3-phosphate (G3P) are dependent on DIR1 for transport to systemic leaves. Closure of stomata, controlled by guard cells, is a local response to bacteria. Here we demonstrate that stomatal response to pathogens is altered in systemic leaves by SAR, and this guard cell SAR defense requires DIR1. Using a multi-omics approach, we have determined potential SAR signaling mechanisms specific for guard cells in systemic leaves by profiling metabolite, lipid, and protein differences between guard cells in wild type and dir1-1 mutant during SAR. We identified two 18C fatty actyls and two 16C wax esters as putative SAR-related molecules dependent on DIR1. Proteins and metabolites related to amino acid biosynthesis and response to stimulus were altered in guard cells of dir1-1 compared to wild type. Identification of guard cell-specific SAR-related molecules will lead to new avenues of genetic modifications/molecular breeding for disease resistant plants.
2022-02-17 | PXD024991 | Pride
Project description:In the absence of adaptive immunity displayed by animals, plants respond locally to biotic challenge via inducible basal defense networks activated through recognition and response toconserved pathogen associated molecular patterns (PAMPs). In addition, immunity can be induced in tissues remote from infection sites via systemic acquired resistance (SAR), initiated following gene-for-gene recognition between plant resistance proteins and microbial effectors.The nature of the mobile signal and remotely activated networks responsible for establishing SAR remain unclear. Here we show that despite the absence of PAMP contact, systemically responding leaves rapidly activate a SAR transcriptional signature with strong similarity to local basal defense. Jasmonates have previously been implicated in systemic signalling in response to wounding and plant herbivory but not SAR. We present several lines of evidence that suggest jasmonates may also be central to SAR. Jasmonic acid (JA) rapidly accumulates in phloem exudates of leaves challenged with an avirulent strain of Pseudomonas syringae. In systemically responding leaves transcripts associated with jasmonate biosynthesis are upregulated and JA increases transiently. SAR can be mimicked by foliar JA application and is abrogated in mutants impaired in jasmonate synthesis or response. We conclude that, jasmonate signalling appears to mediate long-distance information transmission. Moreover, the systemic transcriptional response shares extraordinary overlap with local herbivory and wounding responses, indicating that jasmonates may be central to an evolutionarily conserved signalling network, which decodes multiple abiotic and biotic stress signals. Experimenter name: William Truman; Experimenter phone: +44 (0)1392 263789; Experimenter fax: +44 (0)1392 263434; Experimenter address: School of Biosciences; Experimenter address: Geoffrey Pope Building; Experimenter address: Stocker Road; Experimenter address: Exeter; Experimenter address: Devon; Experimenter zip/postal_code: EX4 4QD; Experimenter country: UK Experiment Overall Design: 9 samples were used in this experiment
2008-06-15 | E-GEOD-6831 | biostudies-arrayexpress
Project description:In the absence of adaptive immunity displayed by animals, plants respond locally to biotic challenge via inducible basal defense networks activated through recognition and response toconserved pathogen associated molecular patterns (PAMPs). In addition, immunity can be induced in tissues remote from infection sites via systemic acquired resistance (SAR), initiated following gene-for-gene recognition between plant resistance proteins and microbial effectors.The nature of the mobile signal and remotely activated networks responsible for establishing SAR remain unclear. Here we show that despite the absence of PAMP contact, systemically responding leaves rapidly activate a SAR transcriptional signature with strong similarity to local basal defense. Jasmonates have previously been implicated in systemic signalling in response to wounding and plant herbivory but not SAR. We present several lines of evidence that suggest jasmonates may also be central to SAR. Jasmonic acid (JA) rapidly accumulates in phloem exudates of leaves challenged with an avirulent strain of Pseudomonas syringae. In systemically responding leaves transcripts associated with jasmonate biosynthesis are upregulated and JA increases transiently. SAR can be mimicked by foliar JA application and is abrogated in mutants impaired in jasmonate synthesis or response. We conclude that, jasmonate signalling appears to mediate long-distance information transmission. Moreover, the systemic transcriptional response shares extraordinary overlap with local herbivory and wounding responses, indicating that jasmonates may be central to an evolutionarily conserved signalling network, which decodes multiple abiotic and biotic stress signals. Experimenter name: William Truman Experimenter phone: +44 (0)1392 263789 Experimenter fax: +44 (0)1392 263434 Experimenter address: School of Biosciences Experimenter address: Geoffrey Pope Building Experimenter address: Stocker Road Experimenter address: Exeter Experimenter address: Devon Experimenter zip/postal_code: EX4 4QD Experimenter country: UK Keywords: infection
2007-01-22 | GSE6831 | GEO
Project description:Systemic Acquired Resistance (SAR) as a plant immune response improves immunity of distal tissue after local exposure to a pathogen. Stomata pores on leaf surfaces are formed by guard cells that recognize bacterial pathogens via pattern recognition receptors. We found that Arabidopsis thaliana plants that have been previously exposed to the pathogenic bacteria Pseudomonas syringae pv. tomato DC3000 (Pst) exhibit an altered stomatal response compared to control plants when systemic leaves are later exposed to the bacteria. Reduced stomatal apertures of SAR primed plants lead to decreases in the number of bacteria that enter the apoplastic space of the leaves. To examine how SAR affects molecular processes in guard cells of distal leaves, we collected Arabidopsis guard cell samples and extracted lipids, metabolites and proteins using a 3-in-1 method. Multi-omic results have revealed molecular components of SAR response specific to the functions of guard cells and roles of ROS and fatty acid signaling in guard cell SAR response. Additionally, our results show an increase in palmitic acid and its derivative 9-PAHSA in primed guard cells. Palmitic acid may play a role as an agonist to Flagellin Sensitive 2 (FLS2), which initiates stomatal closure upon perception of bacterial flagella. The improved understanding of how SAR immune signals affect stomatal movement and immunity can aid biotechnology and marker-based breeding of crops for enhanced disease resistance.
2021-09-09 | PXD022880 | Pride
Project description:Previous studies from our laboratory have shown that the resistance increase observed after biological systemic acquired resistance (SAR) induction in plants can be mimicked by exogenous plant treatment with N-hydroxypipecolic acid (NHP, Hartmann et al., 2018, Schnake et al., 2020). Moreover, exogenous application of the NHP biosynthetic precursor pipecolic acid (Pip) induced a transcriptional response that was overlapping with the SAR transcriptional response and fully depended on the NHP synthase FMO1 (Hartmann et al., 2018; E-MTAB-6243). In order to investigate whether elevations of NHP lead to a SAR-like transcriptional reprogramming, we supplied individual Arabidopsis wildtype Col-0 plants, as well as sid2-1 and npr1-3 mutant plants, with doses of 10 µmol NHP and determined the transcriptional response in leaves 24 hours later on the whole genome level by RNA-sequencing analyses in relation to control-treated (H2O) plants. Col-0 plants were additionally treated with doses of 10 µmol Pip in order to directly compare the transcriptional responses of the foliage between Pip and NHP. Arabidopsis thaliana plants were grown individually in pots containing a mixture of soil, vermiculite and sand (8:1:1) in a controlled cultivation chamber with a 10-h day (9 AM to 7 PM; photon flux density 100 mol m-2 s-1) / 14-h night cycle and a relative humidity of 70 %. Day and night temperatures were set to 21°C and 18°C, respectively. Experiments were performed with 5-week-old, naive plants exhibiting a uniform appearance. Treatments with NHP and Pip were essentially performed as detailed in Hartmann et al. (2018, Cell 173, 456–469). In brief, 10 ml of a 1 mM aqueous solution of NHP or Pip (equates to a dose of 10 µmol) were pipetted onto the soil of individually cultivated plants. 10 ml of water applied in the way served as control treatments. In total, three biologically independent, replicate experiments were performed. In each experiment, 18 full-grown leaves from 6 different plants were pooled 24 hours after the respective treatments for one biological replicate. In this way, 3 biologically independent, replicate samples per treatment and plant genotype were obtained.
2021-05-03 | E-MTAB-10230 | biostudies-arrayexpress
Project description:We investigated the relationships of the two immune-regulatory plant metabolites salicylic acid (SA) and pipecolic acid (Pip) in the establishment of plant systemic acquired resistance (SAR) in Arabidopsis thaliana induced by the bacterial pathogen Pseudomonas syringae. To characterize the transcriptional SAR response, we used wild-type Col-0 plants, SA-deficient sid2 plants and Pip-deficient ald1 plants and performed RNA-sequencing analyses (Bernsdorff et al., Plant Cell, 2016). SAR establishment in the wild-type is characterized by a strong transcriptional response systemically induced in the foliage that prepares plants for future pathogen attack by pre-activating multiple stages of defense signaling. Whereas systemic Pip elevations are indispensable for SAR and necessary for virtually the whole transcriptional SAR response, a moderate but significant SA-independent component of SAR activation and SAR gene expression is revealed. Arabidopsis thaliana plants were grown individually in pots containing a mixture of soil, vermiculite and sand (8:1:1) in a controlled cultivation chamber with a 10-h day (9 AM to 7 PM; photon flux density 100 mol m-2 s-1) / 14-h night cycle and a relative humidity of 70 %. Day and night temperatures were set to 21C and 18C, respectively. Experiments were performed with 5- to 6-week-old, naive plants exhibiting a uniform appearance. To activate SAR, plants were infiltrated between 10 AM and 12 AM into three lower (1) leaves with suspensions of the bacterial pathogen Pseudomonas syringae pv. maculicola (OD600 = 0.005). Infiltration with 10 mM MgCl2 served as the mock-control treatment. Upper (2) leaves were harvested 48 h after the primary treatment for the determination of systemic gene expression by RNA-seq analyses. Three biologically independent, replicate SAR induction experiments were performed with Col-0 and sid2 plants (experimental set 1), and three other biologically independent experiments with Col-0 and ald1 plants (experimental set 2). In each SAR experiment, at least 6 upper (2) leaves from 6 different plants pre-treated in 1 leaves with Psm (MgCl2) were pooled for one biological Psm- (mock-control) replicate. In this way, 3 biologically independent, replicate samples per treatment and plant genotype were obtained within each SAR set.
2015-12-27 | E-MTAB-4151 | biostudies-arrayexpress
Project description:Background. Systemic acquired resistance (SAR) in plants protects against a wide variety of pathogens. Numerous studies in recent decades have focused on induction of SAR, but its molecular mechanism remains largely unknown. Methods. We used a metabolomics approach based on ultra-high-performance liquid chromatographic (UPLC) and mass spectrometric (MS) techniques to identify SAR-related lipid metabolites in an Arabidopsis thaliana model. Multiple statistical analyses were applied for identification of differentially accumulated metabolites. Results. Numerous lipids were implicated as potential factors in plant basal resistance and SAR; these include species of phosphatidic acid (PA), monogalactosyldiacylglycerol (MGDG), phosphatidylcholine (PC), phosphatidylethanolamine (PE), and triacylglycerol (TG). Conclusions. Our findings indicate that lipids accumulated in both local leaves induced for SAR and in systemic leaves during SAR, while others only accumulate in local SAR-induced leaves or in systemic leaves during SAR. These findings will facilitate future studies of molecular basis of SAR
2021-08-18 | PXD027990 |
Project description:Leaf-to-leaf, systemic immune signaling known as systemic acquired resistance (SAR) is poorly understood in monocotyledonous plants. Here, we characterize systemic immunity in barley (Hordeum vulgare) triggered after primary leaf infection with either Pseudomonas syringae pathovar japonica (Psj) or Xanthomonas translucens pathovar cerealis (Xtc). Both pathogens induced resistance in systemic, uninfected leaves against a subsequent challenge infection with Xtc. In contrast to SAR in Arabidopsis thaliana, systemic immunity in barley was not associated with NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 or the local or systemic accumulation of salicylic acid (SA). Instead, we documented a moderate local but not systemic induction of abscisic acid (ABA) after infection of leaves with Psj. In contrast to SA or its functional analog benzothiadiazole, local applications of the jasmonic acid methyl ester or ABA triggered systemic immunity to Xtc. RNA-seq analysis of local and systemic transcript accumulation revealed unique gene expression changes in response to both Psj and Xtc and a clear separation of local from systemic responses. The systemic response appeared relatively modest and quantitative RT-PCR associated systemic immunity with the local and systemic induction of two WRKY and two ETHYLENE RESPONSIVE FACTOR-like transcription factors. Systemic immunity against Xtc was further associated with transcriptional changes after a secondary/systemic Xtc challenge infection; these changes were dependent on the primary treatment. Taken together, bacteria-induced systemic immunity in barley may be mediated in part by WRKY and ERF-like transcription factors possibly facilitating transcriptional reprogramming to potentiate immunity.
2014-11-24 | E-MTAB-3056 | biostudies-arrayexpress