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Accession Number: GSE97641 Platform: GPL17133: [AraGene-1_1-st] Arabidopsis Gene 1.1 ST Array [transcript (gene) version] Organism: Arabidopsis thaliana Published on 2018-01-02 Summary: Increased ambient temperature is widely considered to be inhibitory to basal and effector-triggered plant immunity. For example, SNC1-dependent auto-immunity in Arabidopsis results in enhanced basal resistance at 22ºC, which is fully suppressed at 28ºC. The sumoylation mutant siz1 also displays auto-immunity at 22ºC. We find that its auto-immunity is sustained at 28ºC while still requiring PAD4/EDS1 and SNC1 function. Moreover, its rosette size does not fully recover at 28ºC, which is normally seen for SNC1 gain-of-function mutants. Related, thermomorphogenesis is also compromised in the SUMO mutants. This role of SIZ1 in growth regulation does not depend on PAD4 or SNC1. In corroboration, SUMO mutants show a global delay in their transcriptional profile for thermosensitive growth regulators and these differentially expressed genes show an overrepresentation for PIF4 genomic targets. This transcription factor (TF) PIF4 is the central regulator of thermomorphogenesis, while also inhibiting plant immunity at 28ºC. Our findings thus reveal that SUMO conjugation has a central role in PIF4 regulation prioritizing growth over immunity at elevated temperatures. Such molecular understanding of how temperature affects growth over immunity is important to mitigate the effects of climate change on agriculture This experiment we have examined how gene expression is affected in two SUMO mutants (siz1-2; sumo1 amiR-SUMO1 [aka. sumo1/2KD] ) when the plants are placed at 28C constant ambient temperature, which is a condition normally used to induce thermomorphogenesis. We used as control the pad1-4 background, as the siz1-2 and sumo1/2KD mutants normailly suffer from constitutive defence signalling due hyperaccumulation of SA, which is suppressed by introgression of pad4 in these backgrounds. Overall Design: Three biological replicates per samples; Arabidopsis plants were grown at 22C (t=0) and shifted to 28C (t=24hrs, and t=96 hrs post shift); In total three lines were compared: pad4-1 ('negative' control), siz1-2 pad4-1 double mutant, and sumo1-1 amiR-SUMO2 pad4-1 triple mutant Contact: Name: Martijs Jonker Organization: University of Amsterdam Deparment: Microarray Department Address: Science Park 904 Amsterdam Netherlands Email: m.j.jonker@uva.nl Organization: Affymetrix, Inc. Address: Santa Clara CA 95051 USA Email: geo@ncbi.nlm.nih.gov, support@affymetrix.com Phone: 888-362-2447 Web-Link: http://www.affymetrix.com/index.affx
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Accession Number: GSE44151 Platform: GPL1261: [Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array Organism: Mus musculus Published on 2018-01-02 Summary: The basic helix-loop-helix proteins Olig1 and Olig2 are expressed in high grade, aggressive human glioblastoma multiformes (GBMs). Here we investigated genetic mechanisms regulating Olig1/2 function during gliomagenesis. Although Olig2 function is necessary for early-aggressive tumor formation in a genetically relevant model of classic GBMs with intact p53 function, late-onset gliomas do eventually form. Using an unbiased approach, we identified Id4, encoding a negative HLH protein, as a gene target potently repressed by Olig2 in glioma progenitors. Although Id4 is thought to antagonize proneural genes involved in differentiation, we report a paradoxical role for Id4 in glioma. Genetic deletion of Id4 converts Olig2-/- gliomas to the early-aggressive form, and conversely, overexpression of Id4 inhibits intact Olig2 and prevents even late-onset tumors. Olig1 overexpression is sufficient for gliomagenesis in an Id4-dependent manner.  Together, these findings indicate that gliomagenic factors Olig1 and Olig2 are opposed by Id4 function, which acts as tumor suppressor in p53-intact gliomas. Overall Design: Analysis of the transcriptomes of Olig vs. Olig-deficient gliomagenic progenitor cells. 11 distinct conditions with biological replicates: Olig1/2-/- Ink4a/Arf-/- EGFRvIII cells (n=6), Olig1/2+/- Ink4a/Arf-/- EGFRvIII cells (n=3), Olig1/2+/+ Ink4a/Arf-/- EGFRvIII cells (n=3), Olig1/2-/- Ink4a/Arf-/- EGFRvIII cells overexpressing GFP (n=3), Olig1/2+/- Ink4a/Arf-/- EGFRvIII cells overexpressing GFP (n=2), Olig1/2-/- Ink4a/Arf-/- EGFRvIII cells overexpressing Olig2 (n=3), Olig1/2+/- Ink4a/Arf-/-EGFRvIII cells overexpressing Olig2 (n=2), Olig1/2-/- forebrain E18.5 (n=2), Olig1/2+/- forebrain E18.5 (n=2), Olig1/2-/- spinal cord E18.5 (n=2) and Olig1/2+/- spinal cord E18.5 (n=2). Contact: Name: Alvin T. Kho Organization: Boston Children's Hospital Deparment: Informatics Program Address: 320 Longwood Avenue Boston MA 02115 USA Email: alvin_kho@hms.harvard.edu Phone: 617-919-2182 Organization: Affymetrix, Inc. Address: Santa Clara CA 95051 USA Email: geo@ncbi.nlm.nih.gov, support@affymetrix.com Phone: 888-362-2447 Web-Link: http://www.affymetrix.com/index.affx
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Accession Number: GSE108313 Platform: GPL16791: Illumina HiSeq 2500 (Homo sapiens) Organism: Homo sapiens Published on 2018-01-02 Summary: We reasoned that by using a distinct set of oligo-tagged antibodies against ubiquitously expressed proteins, we could uniquely label multiple populations of cells, multiplex them together, and use the barcoded antibody signal as a fingerprint. We refer to this approach as cellular "hashing", as our set of oligos defines a "look up table" to assign each multiplexed cell to its original sample. We demonstrate application of the technique to combine eight samples and run them simultaneously in a single droplet based scRNA-seq run. We show that cell hashtags allow sample multiplexing, confident multiplet identification and super-loading in the context of a commonly used droplet-based scRNA-seq method to drive down the per-cell cost of large-scale scRNA-seq experiments Overall Design: We chose a set of monoclonal antibodies directed against ubiquitously and highly expressed immune surface markers (CD45, CD98, CD44, and CD11a) and combined these antibodies into eight identical pools (pool A-H), and subsequently conjugated each pool to a distinct hashtag oligonucleotide (henceforth referred to as HTOs). The HTOs contain a unique 10- or 12-bp barcode that could be read out and linked to the cellular transcriptome, through minor modifications to standard scRNA-seq protocols. Contact: Name: Rahul Satija Organization: New York Genome Center Address: 101 Avenue of the Americas New York NY 10013 USA Email: rsatija@nygenome.org Organization: GEO Address: USA
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Accession Number: GSE96743 Platform: GPL15207: [PrimeView] Affymetrix Human Gene Expression Array Organism: Homo sapiens Published on 2018-01-02 Summary: Melanoma patients with high mRNA levels of the HDL receptor SR-BI (SCARB1) reveal poor survival outcome. The aim of the study was to evaluate the role of SR-BI in cancer progression. Therefore, SR-BI was targeted either by siRNA or by using the SR-BI specific lipid transfer inhibitor BLT-1. The SR-BI knockdown specifically revealed reduced protein glycosylation, STAT5 target gene expression and EMT pathway activation. Thus, SR-BI target genes reflect the metastatic phenotype in melanoma cells. We used the transcriptome analysis to compare SR-BI depletion to BLT-1 treatment (which specifically blocks SR-BI mediated lipid transfer) in human melanoma cells. Overall Design: Three human metastasizing melanoma cell lines were treated with BLT-1 or SR-BI siRNA. Thereafter total RNA was isolated and an Affymetrix microarray was performed. Contact: Name: Katharina Kinslechner Organization: Medical University of Vienna Laboratory: Prof. Mario Mikula Deparment: Center of Pathobiochemistry and Genetics Address: Währinger Strasse 10 Vienna Vienna Austria Email: katharina.kinslechner@meduniwien.ac.at Organization: Affymetrix, Inc. Address: Santa Clara CA 95051 USA Email: geo@ncbi.nlm.nih.gov, support@affymetrix.com Phone: 888-362-2447 Web-Link: http://www.affymetrix.com/index.affx
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Accession Number: GSE90153 Platform: GPL17021: Illumina HiSeq 2500 (Mus musculus) Organism: Mus musculus Published on 2018-01-02 Summary: Monocytes, neutrophils and tissue resident macropahges of colon lamina propia are compared to their intratumoral counterparts found in colon adenomas Overall Design: Different myeloid subpopulations were isolated from healthy colon lamina propria and colon adenomas, sorted by flow cytometry and processed for RNA. Contact: Name: Kaibo Duan Organization: Singapore Immunology Network Address: 8A Biomedical Grove, Immunos Building, Level 4 Singapore Singapore Email: duan_kaibo@immunol.a-star.edu.sg Organization: GEO Address: USA
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Accession Number: GSE103693 Platform: GPL15520: Illumina MiSeq (Homo sapiens) Organism: Homo sapiens Published on 2018-01-02 Summary: Arthropod-borne viruses, such as the members of genus Alphavirus, are a significant concern to global public health. As obligate intracellular pathogens, RNA viruses must interact with the host cell machinery to establish, and complete, their viral lifecycles. Despite considerable efforts to define the host/pathogen interactions essential for alphaviral replication, an unbiased and inclusive assessment of alphaviral RNA:protein interactions has not been undertaken. Moreover, the biological and molecular importance of these interactions, in the full context of their molecular function as RNA-binding proteins, has not been fully realized. The data presented here introduces a robust viral RNA:protein discovery method to elucidate the Sindbis virus (SINV) RNA:Protein host interface. Cross-Link Assisted mRNP Purification (CLAMP) assessment reveals an extensive array of host/pathogen interactions centered on the viral RNAs (vRNAs). After prioritization of the host proteins associated with the vRNAs, we identified the site of Protein:vRNA interaction via a CLIP-seq approach and assessed the consequences of the RNA:protein binding event of hnRNP K, hnRNP I, and hnRNP M in regards to viral infection. Herein we demonstrate that mutation of the prioritized hnRNP:vRNA interaction sites effectively disrupted the hnRNP:vRNA interaction. Correlating with disrupted hnRNP:vRNA binding, SINV growth kinetics were reduced relative to wild type parental viral infections in a vertebrate and invertebrate tissue culture models of infection. The molecular mechanism leading to reduced viral growth kinetics was found to be reduced vRNA accumulation and dysregulated structural gene expression. Collectively, this study further defines the scope and importance of the alphavirus host/pathogen vRNA:protein interactions. Overall Design: 5 CLIP-Seq samples in TOTAL- 2 Control Samples (Input and Empty), 3 immunoprecitations of hnRNP proteins (hnRNP K, I and M). Contact: Name: Kevin J Sokoloski Organization: University of Louisville Laboratory: Sokoloski Lab Deparment: Microbiology and Immunology Address: 505 S. Hancock St. Louisville KY 40202 USA Organization: GEO Address: USA
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Accession Number: GSE107684 Platform: GPL15103: Illumina HiSeq 1000 (Mus musculus) Organism: Mus musculus Published on 2018-01-02 Summary: This SuperSeries is composed of the SubSeries listed below. Overall Design: Refer to individual Series Contact: Name: Mario Medvedovic Organization: University of Cincinnati Laboratory: Laboratory for Statistical Genomics and Systems Biology Deparment: Department of Environmental Health Address: 3223 Eden Av. ML 56 Cincinnati OH 45267-0056 USA Organization: GEO Address: USA
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Accession Number: GSE95065 Platform: GPL23080: [HG-U133A_2] Affymetrix Human Genome U133A 2.0 Array (HGU133A2 Hs ENTREZG 19.0.0) Organism: Homo sapiens Published on 2018-01-02 Summary: We used microarrays to explore gene expression in Systemic Sclerosis patients. Overall Design: Compilation of skin biopsies gene expression from patients with diffuse cutaneous systemic sclerosis and healthy controls. Contact: Name: Julio C Mantero Organization: Boston University School of Medicine Deparment: Rheumatology Address: 72 E Concord St Boston MA 02118 USA Name: GEO admin Organization: NCBI/NLM/NIH Address: 9000 Rockville Pike Bethesda MD 20892 USA Email: geo@ncbi.nlm.nih.gov
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Accession Number: GSE95007 Platform: GPL13112: Illumina HiSeq 2000 (Mus musculus) Organism: Mus musculus Published on 2018-01-02 Summary: In mammals, the peptide hormone vasopressin controls renal water excretion, largely through regulation of the molecular water channel aquaporin-2 (AQP2) in the renal collecting duct. Regulatory mechanisms of AQP2 show: 1) short-term regulation by membrane trafficking; and 2) long-term regulation involving vasopressin-induced changes in the abundance of the aquaporin-2 protein. Vasopressin activates a G protein-coupled receptor (V2R) increasing cyclic AMP and activating protein kinase PKA. Crebbp and Ep300 are known targets of PKA. They are histone acetyltransferases that acetylate histone H3 lysine-27, a histone mark associated with open chromatin and increased transcription (Tie F et al. Development 2009). The translocation of CREBBP and Ep300 into the nucleus in response to vasopressin in the collecting duct cells, predicts that vasopressin, working through PKA, may increase histone H3K27 acetylation of some genes. We tested this by performing ChIP-Seq for this modification. Overall Design: To identify changes of Histone modification (acetylation) in response to vasopressin in cultured mouse collecting duct cells (mpkCCD), we carried out ChIP-seq for genome-wide distribution of histone 3 acetylation (H3K27ac) (n=2). Observations were made both after 24-hr treatment with the vasopressin analog dDAVP and with vehicle. Contact: Name: Hyun Jun Jung Organization: NHLBI/NIH Laboratory: Epithelial Systems Biology Lab Deparment: Systems Biology Center Address: 9000 Center Dr. Bldg.10 6N314 Bethesda MD 20892 USA Email: hynjn.jung@gmail.com Organization: GEO Address: USA
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Accession Number: GSE108407 Platform: GPL570: [HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array Organism: Homo sapiens Published on 2018-01-02 Summary: The role of Gata2 in regulating the expression of HLA in human decidual stromal cells Overall Design: Human primary stromal cells from three different patients were grown to approximately 70% confluence and subsequently treated with 100nM medroxyprogesterone acetate, and 1mM 8-bromo-cAMP and transfected with 60nM scrambled, non-targeting (siNT), or GATA2-targeting (siGATA2) siRNA using Lipofectamine RNAiMax lipid per the manufacturer’s instructions. After 72 hours of transfection exposure cells were harvested and RNA isolated using the RNAeasy Mini kit as per manufacterer’s instructions. cRNA labeling was performed according to Agilent Technologies Inc. protocol using the Agilent Quick Amp Labeling Kit following the two-color manufacturer's protocol. Contact: Name: Francesco J DeMayo Organization: National Institute of Environmental Health Sciences Deparment: Reproductive & Developmental Biology Laboratory Address: 111 TW Alexander Drive Research Triangle Park NC 27709 USA Organization: Affymetrix, Inc. Address: Santa Clara CA 95051 USA Email: geo@ncbi.nlm.nih.gov, support@affymetrix.com Phone: 888-362-2447 Web-Link: http://www.affymetrix.com/index.affx
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