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SRP119473
Mus musculus
25 Downloadable Samples
Illumina HiSeq 2500
Description
Polycomb repressive complex 2 (PRC2-EZH2) methylates histone H3 at lysine 27 (H3K27) and is required to maintain gene repression during development. Misregulation of PRC2 is linked to a range of neoplastic malignancies, which is believed to involve methylation of H3K27. However, the full spectrum of non-histone substrates of PRC2 that might also contribute to PRC2 function is not known. We characterized the target recognition specificity of PRC2 and used the resultant data to screen for novel potential targets. The RNA polymerase II (Pol II) transcription factor, Elongin A (EloA), is methylated by PRC2 in vivo. Mutation of the methylated EloA residue decreased repression of many, but not all, PRC2 target genes as measured by both steady state and nascent RNA levels. We propose that PRC2 regulates transcription of a subset of target genes in part via methylation of EloA. Overall design: We examined the transcripitonal profile of EEDnull, EloAnull, EloA mutant, and parental mouse embryonic stem cells by RNAseq. Please note that the .bw processed data file was generated from the *mESC replicate samples together and linked to the corresponding *rep1 sample records.
Publication Title
Polycomb Repressive Complex 2 Methylates Elongin A to Regulate Transcription.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina HiSeq 2500
Description
Polycomb repressive complex 2 (PRC2-EZH2) methylates histone H3 at lysine 27 (H3K27) and is required to maintain gene repression during development. Misregulation of PRC2 is linked to a range of neoplastic malignancies, which is believed to involve methylation of H3K27. However, the full spectrum of non-histone substrates of PRC2 that might also contribute to PRC2 function is not known. We characterized the target recognition specificity of PRC2 and used the resultant data to screen for novel potential targets. The RNA polymerase II (Pol II) transcription factor, Elongin A (EloA), is methylated by PRC2 in vivo. Mutation of the methylated EloA residue decreased repression of many, but not all, PRC2 target genes as measured by both steady state and nascent RNA levels. We propose that PRC2 regulates transcription of a subset of target genes in part via methylation of EloA. Overall design: We examined the nascent transcripiton profile of mES cells by adding 5-Bromouridine (BrU) to the media for 10 min. Following RNA isolation, BrU-labelled nascent RNA species were affinity purified using BrdU antibody and sequenced after library preparation. Please note that each .bw file was generated from two replicate samples together and linked to the corresponding *rep1 sample records.
Publication Title
Polycomb Repressive Complex 2 Methylates Elongin A to Regulate Transcription.
Sample Metadata Fields
Specimen part, Subject
View Samples- Caenorhabditis elegans
- 9 Downloadable Samples
Affymetrix C. elegans Genome Array (celegans)
Description
Many pathogens secrete toxins that target key host processes resulting in the activation of immune pathways. The secreted Pseudomonas aeruginosa toxin Exotoxin A (ToxA) disrupts intestinal protein synthesis which triggers the induction of a subset of P. aeruginosa-response genes in the nematode Caenorhabditis elegans. We found that losing one ToxA-induced C. elegans gene, the Tribbles pseudokinase ortholog nipi-3, results in hypersusceptibility to both P. aeruginosa and ToxA. We determined that NIPI-3 mediates the post-developmental expression of intestinal immune genes and proteins and primarily functions in parallel to known immune pathways, including p38 PMK-1 MAPK signaling. Here we present the microarray data that was used to determine that (1) nipi-3 regulates immune gene expression and that (2) nipi-3 and pmk-1 regulate non-overlapping gene sets consistent with them functioning in parallel.
Publication Title
Tribbles ortholog NIPI-3 and bZIP transcription factor CEBP-1 regulate a Caenorhabditis elegans intestinal immune surveillance pathway.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Celiac disease (CeD) is an intestinal immune-mediated disorder caused by gluten ingestion in genetically predisposed subjects. CeD is characterized by villous atrophy, altered intestinal permeability, crypt hyperplasia and innate and adaptive immune response. This study aimed to develop and validate the use of intestinal organoids from celiac patients to study CeD. A repository of organoids from duodenum of non-celiac and celiac patients was generated and characterized accordingly to standard procedures. RNA-seq analysis was employed to study the global gene expression program of CeD (n=3) and non-CeD (n=3) organoids sets. While the three celiac derived organoids shared similar transcriptional signatures the NC samples set appeared more heterogeneous. We found 486 genes differentially expressed between the two groups. Of them, 299 genes were downregulated (FC<2; FDR<0.05) and 187 were upregulated in CeD (FC >2; FDR<0.05). We observed CeD organoids had significantly altered expression of genes associated with barrier function, innate immunity, and stem cell function. Overall design: mRNA profiles of 3 non-celiac healthy controls and 3 celiac organoids derived from duodenal biopsies.
Publication Title
Human gut derived-organoids provide model to study gluten response and effects of microbiota-derived molecules in celiac disease.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- NextSeq 500
Description
Profiling of the transcriptome of FITChigh/FSCdim and FITCdim/FSChigh sub-populations. Three biological replicates were profiled for each cell type. Overall design: Profiling of the transcriptome of FITChigh/FSCdim and FITCdim/FSChigh sub-populations. Three biological replicates were profiled for each cell type.
Publication Title
An autofluorescence-based method for the isolation of highly purified ventricular cardiomyocytes.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000, NextSeq 500
Description
Methylation at 5-cytosine (5-mC) is a fundamental epigenetic DNA modification associated recently with cardiac disease. In contrast, the role of 5-hydroxymethylcytosine (5-hmC) – 5-mC's oxidation product – is unknown in the context of the heart. Here, we assess the hydroxymethylome in embryonic, neonatal, adult and hypertrophic mouse cardiomyocytes, showing that dynamic modulation of hydroxymethylated DNA is associated with specific transcriptional networks during heart development and failure. DNA hydroxymethylation marks gene bodies of highly expressed genes and distal regulatory regions with enhanced activity. Pathological hypertrophy is characterized by a partial shift towards a fetal-like distribution pattern. We further demonstrate a regulatory function of TET2 and provide evidence that the expression of key cardiac genes, such as Myh7 is modulated by TET2-mediated 5-hmC deposition on the gene body and at enhancers in cardiac cells. We thus provide the first genome-wide analysis of 5-hmC in the cardiomyocyte, and establish the role of this epigenetic modification in heart development and disease Overall design: Profiling of the transcriptome of embryonic, neonatal, adult, 1 week hypertrophic cardiomyocytes, sh-control and sh-TET2 cardiomyocytes. Two biological replicates were profiled for each cell type.
Publication Title
DNA hydroxymethylation controls cardiomyocyte gene expression in development and hypertrophy.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 73 Downloadable Samples
- Illumina HiSeq 2500
Description
CD33-/- and/or TREM2-/- mice were crossed with the 5xFAD mouse model of Alzheimer's disease to generate single and double CD33/TREM2 knock-out mice on 5xFAD background. Transcriptome and gene expression analyses were performed to analyze the impact of CD33 and/or TREM2 knock-out on the transcriptome of microglia in the context of amyloid pathology. The results revealed that CD33 and/or TREM2 knock-out reprogrammed microglial gene expression signatures in 5xFAD mice in an age-dependent manner. Differential gene expression in 5xFAD;CD33-/- microglia depended on the presence of TREM2. These data suggest that TREM2 acts downstream of CD33. Overall design: Microglia were isolated from brains of WT, 5xFAD, 5xFAD;CD33-/-, 5xFAD;TREM2-/-, and 5xFAD;CD33-/-;TREM2-/- mice at 4 and 8 months of age, using FACS sorting for CD11b and CD45. RNA was extracted using the RNeasy Plus Micro Kit (Qiagen). Libraries were prepared using the TruSeq Stranded mRNA LT Prep Kit (Illumina) and sequenced on an Illumina HiSeq 2500 sequencer using single-end 50. Reads were aligned to mouse genome mm10 using the STAR aligner. Read counts for individual genes were obtained using HTSeq.
Publication Title
TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease.
Sample Metadata Fields
Age, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: mRNA profiles of Sox2 WT and Sox2 KO gastric glands were generated by RNA-sequencing, in triplicate, using a Illumina HiSeq 2500 instrument, resulting in 36 million single-end 50bp reads per smaple. Sequencing reads were mapped to the mouse reference genome (mm10/GRCm38) using STAR (Dobin et al., 2013). Read counts over transcripts were calculated using HTSeq v.0.6.0 (Anders et al., 2015) based on a current Ensembl annotation file for mm10/GRCm38 (release 75). Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of cancer and intestinal related genes. Overall design: mRNA profiles of stomachs from 10 week old Sox2 WT and Sox2 KO mice were generated by sequencing, in triplicate, using a Illumina HiSeq 2500.
Publication Title
Sox2 Suppresses Gastric Tumorigenesis in Mice.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina Genome Analyzer
Description
Natural killer (NK) cells play a critical role in early host defense to infected and transformed cells. Here we show that mice deficient in Eri1, a conserved 3’-to-5’ exoribonuclease that represses RNA interference, have a cell-intrinsic defect in NK cell development and maturation. Eri1–/– NK cells displayed delayed acquisition of Ly49 receptors in the bone marrow and a selective reduction in Ly49D and Ly49H activating receptors in the periphery. Eri1 was required for immune-mediated control of mouse cytomegalovirus (MCMV) infection. Ly49H+ NK cells deficient in Eri1 failed to expand efficiently during MCMV infection, and virus-specific responses were also diminished among Eri1–/– T cells. We identified miRNAs as the major endogenous small RNA target of Eri1 in mouse lymphocytes. Both NK and T cells deficient in Eri1 displayed a global, sequence-independent increase in miRNA abundance. Ectopic Eri1 expression rescued defective miRNA expression in mature Eri1–/– T cells. Thus, mouse Eri1 regulates miRNA homeostasis in lymphocytes and is required for normal NK cell development and anti-viral immunity. Overall design: Small RNA profiling from wildtype and Eri1-deficient mouse CD4+ T cells
Publication Title
Eri1 regulates microRNA homeostasis and mouse lymphocyte development and antiviral function.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This file contains gene microarray data from subsets of human intestinal dendritic cells, as defined by their expression of CD103 and Sirpa. This will allow for better understanding of human intestinal DC subsets in general and will facilitate translation from findings in the mouse.
Publication Title
Comparative transcriptional and functional profiling defines conserved programs of intestinal DC differentiation in humans and mice.
Sample Metadata Fields
Specimen part
View Samples