Plant defenses against pathogens and insects are regulated differentially by cross-communicating signaling pathways in which salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) play key roles. To understand how plants integrate pathogen- and insect-induced signals into specific defense responses, we monitored the dynamics of SA, JA, and ET signaling in Arabidopsis after attack by a set of microbial pathogens and herbivorous insects with different modes of attack. Arabidopsis plants were exposed to a pathogenic leaf bacterium (Pseudomonas syringae pv. tomato), a pathogenic leaf fungus (Alternaria brassicicola), tissue-chewing caterpillars (Pieris rapae), cell-content-feeding thrips (Frankliniella occidentalis), or phloem-feeding aphids (Myzus persicae). Monitoring the signal signature in each plant-attacker combination showed that the kinetics of SA, JA, and ET production varies greatly in both quantity and timing. Analysis of global gene expression profiles demonstrated that the signal signature characteristic of each Arabidopsis-attacker combination is orchestrated into a surprisingly complex set of transcriptional alterations in which, in all cases, stress-related genes are overrepresented. Comparison of the transcript profiles revealed that consistent changes induced by pathogens and insects with very different modes of attack can show considerable overlap. Of all consistent changes induced by A. brassicicola, P. rapae, and F. occidentalis, more than 50% were also induced consistently by P. syringae. Notably, although these four attackers all stimulated JA biosynthesis, the majority of the changes in JA-responsive gene expression were attacker-specific. All together our study shows that SA, JA, and ET play a primary role in the orchestration of the plant's defense response, but other regulatory mechanisms, such as pathway cross-talk or additional attacker-induced signals, eventually shape the highly complex attacker-specific defense response.
Signal signature and transcriptome changes of Arabidopsis during pathogen and insect attack.
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View SamplesPurpose: Identify zebrafish microglia transcriptome in the healthy and neurodegenerative brain. Methods: RNA sequencing was performed on FACS-sorted microglia (3x), other brain cells (3x) and activated microglia (4x). Microglia activation was induced using nitroreductase-mediated cell ablation. 10-20 million reads per sample were obtained. Reads were mapped to zebrafish genome GRC10. Results: We identified the zebrafish microglia transcriptome, which shows overlap with previously identified mouse microglia transcriptomes. Transcriptomes obtained 24h and 48h after treatment appeared highly similar. Therefore, these datasets were pooled. Additionally, we identified an acute proliferative response of microglia to induced neuronal cell death. Overall design: Zebrafish microglia transcriptomes of homeostatic microglia (triplicate), other brain cells (triplicate), activated microglia 24h (duplo), activated microglia 48h (duplo). In data analysis all activated microglia samples were pooled.
Identification of a conserved and acute neurodegeneration-specific microglial transcriptome in the zebrafish.
No sample metadata fields
View SamplesThe goal of this RNA-Seq analysis was to identify genes differentially expressed in a C. elegans strain overexpressing HSP-90 in the neurons compared to control (N2) animals. C. elegans overexpressing HSP-90 protein in the neurons activate transcellular chaperone signalling that enhances organismal proteostasis. This study aimed to identify components of the signalling pathway responsible for this effect. Overall design: Gene expression profile of L4 C. elegans wild type (N2) animals compared to L4 C. elegans overexpressing HSP-90::GFP in the neurons, using a neuron-specific promoter (F25B3.3p), grown at 20C. 3 replicates of each sample.
A PQM-1-Mediated Response Triggers Transcellular Chaperone Signaling and Regulates Organismal Proteostasis.
Cell line, Subject
View SamplesHeparan sulfate (HS), a long linear polysaccharide, is implicated in various steps of tumorigenesis, including angiogenesis. We successfully interfered with HS biosynthesis using a peracetylated 4-deoxy analog of the HS constituent GlcNAc and studied the compounds metabolic fate and its effect on angiogenesis. The 4-deoxy analog was activated intracellularly into UDP-4-deoxy-GlcNAc and HS expression was inhibited up to ~96% (IC50 = 16 M). HS chain size was reduced, without detectable incorporation of the 4-deoxy analog, likely due to reduced levels of UDP-GlcNAc and/or inhibition of glycosyltransferase activity. Comprehensive gene expression analysis revealed reduced expression of genes regulated by HS binding growth factors as FGF-2 and VEGF. Cellular binding and signaling of these angiogenic factors was inhibited. Micro-injection in zebrafish embryos strongly reduced HS biosynthesis, and angiogenesis was inhibited in both zebrafish and chicken model systems. All these data identify 4-deoxy-GlcNAc as a potent inhibitor of HS synthesis which hampers pro-angiogenic signaling and neo-vessel formation.
Interfering with UDP-GlcNAc metabolism and heparan sulfate expression using a sugar analogue reduces angiogenesis.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of naive pluripotency.
Sex, Specimen part, Treatment
View SamplesThis microarray was performed to gain insight in the effect of GY118F stimulation in EpiSCs. This array is part of the following paper to be published in Nature Communications: JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of nave pluripotency by Anouk L. van Oosten, Yael Costa, Austin Smith & Jos C.R. Silva
JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of naive pluripotency.
Specimen part, Treatment
View SamplesThis microarray was performed to gain insight in the downstream targets of GY118F in iPS cells. This array is part of the following paper to be published in Nature Communications: JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of nave pluripotency by Anouk L. van Oosten, Yael Costa, Austin Smith & Jos C.R. Silva
JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of naive pluripotency.
Sex, Specimen part, Treatment
View SamplesEarly perturbations in vascular health can be detected by imposing subjects to a high fat (HF) challenge and measure response capacity. Subtle responses can be determined by assessment of whole-genome transcriptional changes. We aimed to magnify differences in health by comparing gene-expression changes in peripheral blood mononuclear cells (PBMCs) towards a high MUFA or SFA challenge between subjects with different cardiovascular disease risk profiles and to identify fatty-acid specific gene-expression pathways.
High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects.
Sex, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Reprogramming capacity of Nanog is functionally conserved in vertebrates and resides in a unique homeodomain.
Specimen part
View SamplesNanog null neural stem (NS) cells were reprogrammed to naive pluripotency in 2i/LIF conditions with mouse (m) Nanog and human (h) Nanog. Global gene expression in resulting iPS cells was compared to embryonic stem (ES) cells and nanog null NS cells.
Reprogramming capacity of Nanog is functionally conserved in vertebrates and resides in a unique homeodomain.
Specimen part
View Samples