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GSE61399
Homo sapiens
29 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Th1/Th17-type T-cell responses are upregulated in Behcets disease (BD). However, signaling pathways associated with this aberrant immune response are not clarified. Whole-genome microarray profiling was performed with human U133 (Plus 2.0) chips using mRNA of isolated CD14+ monocytes and CD4+ T-cells from PBMC in patients with BD (n=9) and healthy controls (HC) (n=9). Flow cytometric analysis of unstimulated (US) and stimulated (PHA) STAT3 and pSTAT3 expressions of PBMCs were also analysed (BD and HC, both n=26). JAK1 was observed to be upregulated in both CD14+ monocytes (1.94 fold) and CD4+ T-lymphocytes (1.40 fold) of BD patients. Using canonical pathway enrichment analysis, JAK/STAT signaling was identified as activated in both CD14+ monocytes (p=2.95E-06) and in CD4+ lymphocytes (p=8.13E-04) in BD. Interferon (p=1.02E-07) and IL-6 (p=8.91E-03) signaling pathways were also prominent in CD14+ monocytes. Basal unstimulated total STAT3 expression was significantly higher in BD (1.2 vs 3.45, p<0.05). The JAK1/STAT3 signaling pathway is activated in BD, possibly through the activation of Th1/Th17-type cytokines such as IL-2, IFN, IL-6, IL-17 and IL-23.
Publication Title
Activation of the JAK/STAT pathway in Behcet's disease.
Sample Metadata Fields
Specimen part, Disease
View Samples- Drosophila melanogaster
- 4 Downloadable Samples
Illumina Genome Analyzer IIx
Description
Drosophila S2 cells were treated with Heat-shock protein 90 (Hsp90) inhibitor radicicol for 15min, 30min and 1h. Poly(A) RNA was isolated and sequenced. Overall design: Kinetics of transcriptional response to Hsp90 inhibition
Publication Title
Hsp90 globally targets paused RNA polymerase to regulate gene expression in response to environmental stimuli.
Sample Metadata Fields
Specimen part, Cell line, Subject, Time
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Neural precursor cells (NPCs) are multipotent cells that can generate neurons, astrocytes, and oligodendrocytes in the mammalian central nervous system. Although Zbtb20 was expressed in NPCs, its functions in neural development are not fully understood. We performed microarray analysis to examine changes in gene expression between control and Zbtb20-overexpressed NPCs.
Publication Title
Zbtb20 promotes astrocytogenesis during neocortical development.
Sample Metadata Fields
Specimen part
View Samples- Oryza sativa
- 12 Downloadable Samples
- Affymetrix Rice Genome Array (rice)
Description
Magnaporthe oryzae causes rice blast, the most devastating foliar fungal disease of cultivated rice. During disease development the fungus simultaneously maintains both biotrophic and necrotrophic growth corresponding to a hemi-biotrophic life style. The ability of M. oryzae to also colonize roots and subsequently develop blast symptoms on aerial tissue has been recognized. The fungal root infection strategy and the respective host responses are currently unknown. Global temporal expression analysis suggested a purely biotrophic infection process reflected by the rapid induction of defense response-associated genes at the early stage of root invasion and subsequent repression coinciding with the onset of intracellular fungal growth. The same group of down-regulated defense genes was increasingly induced upon leaf infection by M. oryzae where symptom development occurs shortly post tissue penetration. Our molecular analysis therefore demonstrates the existence of fundamentally different tissue-specific fungal infection strategies and provides the basis for enhancing our understanding of the pathogen life style.
Publication Title
Tissue-adapted invasion strategies of the rice blast fungus Magnaporthe oryzae.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
- Illumina HiSeq 2000, Illumina Genome Analyzer IIx
Description
The Photo-Activatable Ribonucleoside-enhanced CrossLinking and ImmunoPrecipitation (PAR-CLIP) method was recently developed for global identification of RNAs interacting with proteins. The strength of this versatile method results from induction of specific T to C transitions at sites of interaction. However, current analytical tools do not distinguish between non-experimentally and experimentally induced transitions. Furthermore, geometric properties at potential binding sites are not taken into account. To surmount these shortcomings, we developed a two-step algorithm consisting of a non-parametric two-component mixture model and a wavelet-based peak calling procedure. Our algorithm can reduce the number of false positives up to 24% thereby identifying high confidence interaction sites. We successfully employed this approach in conjunction with a modified PAR-CLIP protocol to study the functional role of nuclear MOV10, a putative RNA helicase interacting with Argonaute2 and Polycomb. Our method, available as the R package wavClusteR, is generally applicable to any substitution-based inference problem in genomics. Overall design: The data comprises one MOV10 PAR-CLIP data file and one nuclear RNA-seq file
Publication Title
Mixture models and wavelet transforms reveal high confidence RNA-protein interaction sites in MOV10 PAR-CLIP data.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2000
Description
The molecular chaperone heat shock protein 90 (HSP90) is thought to buffer genetic variation uncoupling phenotypic outcome from individual genotypes. HSP90 thus acts as an evolutionary capacitor by facilitating an accumulation of natural genetic variation. The molecular mechanism underlying the buffering ability is unclear, and HSP90-contingent genetic variation maps both to coding and non-coding parts of the genome. Our genome-wide data indicate that a compromised chaperoning activity of HSP90 causes derepression of endogenous retroviruses (ERVs) in mouse somatic cells. This results in an upregulation of host genes located in the neighborhood of pre-existing ERVs insertion sites. We provide genetic and biochemical evidence that HSP90 cooperates with KAP1/ SETDB1 histone methyltranferase pathway to repress ERVs. Individual mouse strains have unique integration sites of ERVs in their genomes. Consequently distinct genes are responsive to HSP90 inhibitor in different mouse strains depending on the position of the genes vis-Ã -vis strain-specific ERV insertion sites. Since ERVs have been exapted to drive novel transcriptional networks during mammalian evolution, HSP90 may have acted as a capacitor by buffering variation caused by ERV in non-coding regions of the genome. Our studies provide the first molecular framework by which HSP90 can mitigate genetic variation in gene-regulatory regions affecting gene expression and phenotypes. Overall design: We have performed RNA-seq in mouse embryonic stem cells, neuronal progenitor cells and bone-marrow-derived macrophages treated with NVP-AUY922 in triplicates.
Publication Title
The evolutionary capacitor HSP90 buffers the regulatory effects of mammalian endogenous retroviruses.
Sample Metadata Fields
Specimen part, Subject
View Samples- Arabidopsis thaliana
- 4 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Analysis of sol2 mutant. SOL2 protein is a receptor-like kinase
Publication Title
The receptor-like kinase SOL2 mediates CLE signaling in Arabidopsis.
Sample Metadata Fields
No sample metadata fields
View Samples- Danio rerio
- 24 Downloadable Samples
- IlluminaHiSeq2500
Description
We report RNA-sequencing data from zebrafish embryos lacking both maternal and zygotic expression of udu (which encodes Gon4l) (MZudu) at tailbud (TB) stage. Transcripts were compared to stage-matched wild-type (WT) embryos to identify differentially expressed genes. Overall design: Sequencing of polyadenylated mRNAs from MZudu mutant and control WT embryos with 2 biological and 2 technical replicates per genotype - each with 3 lanes per sample.
Publication Title
Gon4l regulates notochord boundary formation and cell polarity underlying axis extension by repressing adhesion genes.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Productive rearrangement of the immunoglobulin heavy chain locus triggers a major developmental checkpoint that promotes limited clonal expansion of pre-B cells, culminating in cell cycle arrest and rearrangement of the kappa () or lambda () light-chain loci. B lineage cells lacking the related transcription factors IRF-4 and IRF-8 undergo a developmental arrest at the cycling pre-B cell stage and are blocked for light-chain recombination. Using Irf-4,8-/- pre-B cells we demonstrate that two pathways converge to synergistically drive light-chain rearrangement, a process that is not simply activated by cell cycle exit. One pathway is directly dependent on IRF-4, whose expression is elevated by pre-BCR signaling. IRF-4 targets the 3 and enhancers to increase locus accessibility and positions a kappa allele away from pericentromeric heterochromatin. The other pathway is triggered by attenuation of IL-7 signaling and results in activation of the intronic enhancer via binding of the transcription factor, E2A. Intriguingly, IRF-4 regulates the expression of CXCR4 and promotes the migration of pre-B cells in response to the chemokine CXCL12. We propose that IRF-4 coordinates the two pathways regulating light-chain recombination by positioning pre-B cells away from IL-7 expressing stromal cells.
Publication Title
Regulation of immunoglobulin light-chain recombination by the transcription factor IRF-4 and the attenuation of interleukin-7 signaling.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Plasmacytoid dendritic cells (pDCs) rapidly produce type I interferon (IFN-I) in response to viruses and are essential for antiviral immune responses. Although related to classical dendritic cells (cDCs) in their development and expression profile, pDCs possess many distinct features. Unlike cDCs, pDCs develop in the bone marrow (BM) and emerge into peripheral lymphoid organs and tissues as fully differentiated cells. We now report that pDCs specifically express Runx2, a Runt family transcription factor that is essential for bone development. Runx2-deficient murine pDCs developed normally in the BM but were greatly reduced in the periphery. The defect was cell-intrinsic and was associated with the retention of mature Ly49Q+ pDCs in the BM. Runx2 was required for the expression of several pDC-enriched genes including chemokine receptors Ccr2 and Ccr5. Mature pDCs expressed high levels of Ccr5 at the surface, and Ccr5-deficient pDCs in a competitive setting were reduced in the periphery relative to the BM. Thus, Runx2 is required for the emergence of mature BM pDCs into the periphery, in a process that is partially dependent on Ccr5. These results establish Runx2 as a lineage-specific regulator of immune system development.
Publication Title
Transcription factor Runx2 controls the development and migration of plasmacytoid dendritic cells.
Sample Metadata Fields
Specimen part
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