Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

53 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of seven consecutive stages of mouse thymocyte development

ABSTRACT: Expression profiles of seven consecutive stages of mouse thymocyte development were generated.

ORGANISM(S): Mus musculus

SUBMITTER: Reinhard Hoffmann

PROVIDER: E-GEOD-272 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Rules for gene usage inferred from a comparison of large-scale gene expression profiles of T and B lymphocyte development.

Hoffmann Reinhard R Bruno Ludovica L Seidl Thomas T Rolink Antonius A Melchers Fritz F

Journal of immunology (Baltimore, Md. : 1950) 20030201 3

Ribonucleic acid expression profiles of seven consecutive stages of mouse thymocyte development were generated on high density oligonucleotide arrays. Previously known expression patterns of several genes were confirmed. Ten percent (1,304 of more than 13,000) of the monitored genes were found with 99% confidence to be differentially expressed across all T cell developmental stages. When compared with 1,204 genes differentially expressed in five consecutive B lineage developmental stages of bone ...[more]

PMID: 12538694

Similar Datasets

Dynamic Transformations of Genome-wide Epigenetic Marking and Transcriptional Control Establish T Cell Identity [ChIP-Seq]

Project description:T cell development comprises a stepwise process of commitment from a multipotent precursor. To define molecular mechanisms controlling this progression, we probed five stages spanning the commitment process using deep sequencing RNA-seq and ChIP-seq methods to track genome-wide shifts in transcription, cohorts of active transcription factor genes, histone modifications at diverse classes of cis-regulatory elements, and binding patterns of GATA-3 and PU.1, transcription factors with complementary roles in T-cell development. The results locate potential promoter-distal cis-elements in play and reveal both activation sites and diverse mechanisms of repression that silence genes used in alternative lineages. Histone marking is dynamic and reversible, and while permissive marks anticipate, repressive marks often lag behind changes in transcription. In vivo binding of PU.1 and GATA-3 relative to epigenetic marking reveals distinctive, factor-specific rules for recruitment of these crucial transcription factors to different subsets of their potential sites, dependent on dose and developmental context.M-BM- Genome-wide expression profiles, global distributions of three different histone modifications, and global occupancies of two transcription factors were examined in five developmentally related immature T populations. High throughput sequencing generated on average 9-30 million of mappable reads (single-read) for each ChIP-seq sample, and 10-15 million (single-read) for RNA-seq. Independent biological replicates were analyzed for individual populations. Terminology: while FLDN1_H3Ac_sample1.1 and FLDN1_H3Ac_sample1.2 are two lanes from the same sample, FLDN1_H3Ac_sample1.X and FLDN1_H3Ac_sample2 are from independent biological replicates. The sequence data of the input DNA from the same cell type was used as ChIP-seq background control.

2012-04-13 | E-GEOD-31233 | biostudies-arrayexpress

Dynamic Transformations of Genome-wide Epigenetic Marking and Transcriptional Control Establish T Cell Identity [RNA-Seq]

Project description:T cell development comprises a stepwise process of commitment from a multipotent precursor. To define molecular mechanisms controlling this progression, we probed five stages spanning the commitment process using deep sequencing RNA-seq and ChIP-seq methods to track genome-wide shifts in transcription, cohorts of active transcription factor genes, histone modifications at diverse classes of cis-regulatory elements, and binding patterns of GATA-3 and PU.1, transcription factors with complementary roles in T-cell development. The results locate potential promoter-distal cis-elements in play and reveal both activation sites and diverse mechanisms of repression that silence genes used in alternative lineages. Histone marking is dynamic and reversible, and while permissive marks anticipate, repressive marks often lag behind changes in transcription. In vivo binding of PU.1 and GATA-3 relative to epigenetic marking reveals distinctive, factor-specific rules for recruitment of these crucial transcription factors to different subsets of their potential sites, dependent on dose and developmental context. Genome-wide expression profiles, global distributions of three different histone modifications, and global occupancies of two transcription factors were examined in five developmentally related immature T populations. High throughput sequencing generated on average 9-30 million of mappable reads (single-read) for each ChIP-seq sample, and 10-15 million (single-read) for RNA-seq. Independent biological replicates were analyzed for individual populations. Terminology: FLDN1_RNA-seq_sample1 and FLDN1_RNA-seq_sample2 are independent biological replicates for the same cell type.

2012-04-13 | E-GEOD-31234 | biostudies-arrayexpress

Dynamic Transformations of Genome-wide Epigenetic Marking and Transcriptional Control Establish T Cell Identity

Project description:This SuperSeries is composed of the following subset Series: GSE31233: Dynamic transformations of epigenetic marking and genome-wide transcriptional regulation that establish T cell identity [ChIP-Seq] GSE31234: Dynamic transformations of epigenetic marking and genome-wide transcriptional regulation that establish T cell identity [RNA-Seq] Refer to individual Series

2012-04-13 | E-GEOD-31235 | biostudies-arrayexpress

Generation and purification of Th1 and Th2 effector and memory CD4+ T cells

Project description:NaÃ¯ve CD4+ T cells were isolated from spleen of AND TcR transgenic/green fluorescence protein (GFP) transgenic mice (Kaye et al., Nature 1989;341:746, Wright et al, Blood 2001;97:2278) that recognize a peptide of pigeon cytochrome C in the context of I-Ek and express CD44lo, CD62Lhi, CD45RBhi, and CD25-. After 4 days in vitro stimulation with antigen presenting cells (APC) under either Th1 or Th2 condition, naÃ¯ve cells become Th1 or Th2 effector cells expressing CD44hi, CD62L lo, CD45RBhi, and CD25+. Additional 3 days culture in the absence of APC, those effector cells become rested expressing a phenotype similar to memory cells (CD44 hi, CD62L lo, CD45RB lo and CD25-). These rested effector cells were adaptively transferred into thymectomized, lethally irradiated, and T cell depleted bone marrow reconstituted mice and memory cells were isolated after 4-12 weeks by flow sort. Generation and purification of Th1 and Th2 effector and memory CD4+ T cells of 42 samples.

2010-06-10 | E-GEOD-8352 | biostudies-arrayexpress

C57BL/6J mice B and T cell LC-MSMS study

Project description:Proteome isolated from C57BL/6J mouse B and T cells are evluated for the presence of novel open reading frame products (nORFs). Translation products encoded by non canonical or novel open reading frame (ORF) genomic regions are generally considered too small to play any significant biological role, and dismissed as inconsequential. We conduct a systematic study of novel ORFs to gain new insights into normal biological and disease processes.

2021-09-09 | PXD022099 | Pride

Critical role of histone demethylase Jmjd3 in the regulation of CD4+ T cell differentiation

Project description:Epigenetic factors have been implicated in the regulation of CD4(+) T-cell differentiation. Jmjd3 plays a role in many biological processes, but its in vivo function in T-cell differentiation remains unknown. Here we report that Jmjd3 ablation promotes CD4(+) T-cell differentiation into Th2 and Th17 cells in the small intestine and colon, and inhibits T-cell differentiation into Th1 cells under different cytokine-polarizing conditions and in a Th1-dependent colitis model. Jmjd3 deficiency also restrains the plasticity of the conversion of Th2, Th17 or Treg cells to Th1 cells. The skewing of T-cell differentiation is concomitant with changes in the expression of key transcription factors and cytokines. H3K27me3 and H3K4me3 levels in Jmjd3-deficient cells are correlated with altered gene expression through interactions with specific transcription factors. Our results identify Jmjd3 as an epigenetic factor in T-cell differentiation via changes in histone methylation and target gene expression. ChIP-seq of histone modification marks H3K4me3 and H3K27me3 in WT and JMJD3 cKO mouse CD4+ T-cells

2015-06-13 | E-GEOD-58775 | biostudies-arrayexpress

Asynchronous combinatorial action of four regulatory factors activates Bcl11b for T cell commitment

Project description:During T cell development, multipotent progenitors relinquish competence for other fates and commit to the T cell lineage by turning on Bcl11b, which encodes a transcription factor. To clarify lineage commitment mechanisms, we followed developing T cells at the single-cell level using Bcl11b knock-in fluorescent reporter mice. Notch signaling and Notch activated transcription factors collaborate to activate Bcl11b expression irrespectively of Notch-dependent proliferation. These inputs work via three distinct, asynchronous mechanisms: an early locus âpoisingâ function dependent on TCF-1 and GATA-3, a stochastic-permissivity function dependent on Notch signaling, and a separate amplitude-control function dependent on Runx1, a factor already present in multipotent progenitors. Despite their necessity for Bcl11b activation, these inputs act in a stage specific manner, providing a multitiered mechanism for developmental gene regulation. Two sets of samples were generated from DN T-cell sub-populations derived from culture of bone marrow progenitors from mice containing a knock-in Bcl11b-YFP reporter

2016-06-27 | E-GEOD-76606 | biostudies-arrayexpress

Transcription profiling of mouse naive T cells from T-cell specific furin knockouts and wild type littermates

Project description:Purified naive (CD4+ CD62L+ CD44-) T cells from 10-11 weeks old T cell specific Furin knockout (CD4-cre fur flox/flox) and littermate wild type (fur flox/flox) control mice were profiled for gene expression using Affymetrix MOE 430 2.0 microarray platform.

2008-06-27 | E-MEXP-1682 | biostudies-arrayexpress

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development [ChIP-Seq]

Project description:In immune responses, activated T cells migrate to B cell follicles and develop to T follicular helper (Tfh) cells, a new subset of CD4+ T cells specialized in providing help to B lymphocytes in the induction of germinal centers 1-3. Although Bcl6 has been shown to be essential in Tfh cell function, it may not regulate the initial migration of T cells 4 or the induction of Tfh program as exampled by CXCR5 upregulation 5. Here, we show that the Achaete-Scute homologue 2 (Ascl2) gene that encodes a basic helix-loop-helix (bHLH) transcription factor 6, is selectively upregulated in its expression in Tfh cells. Ectopic expression of Ascl2 uniquely upregulates CXCR5 but not Bcl6 and downregulates CCR7 expression in T cells in vitro and accelerates T cell migration to the follicles and Tfh cell development in vivo. Combined transcriptome profiling and genome-wide occupancy analysis indicate that Ascl2 directly regulates Tfh-related genes while inhibits expression of Th1 and Th17 genes. Acute deletion of Ascl2 as well as blockade of its function with the Id3 protein in peripheral CD4+ T cells results in a failure in Tfh cell development and the germinal center response. Conversely, mutation of Id3, known to cause antibody-mediated autoimmunity, greatly enhances Tfh cell generation. Thus, Ascl2 critically and directly initiates Tfh cell development. Decide Ascl2 binding sites in CD4+ T cells

2014-01-01 | E-GEOD-52839 | biostudies-arrayexpress

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-01 | E-GEOD-52840 | biostudies-arrayexpress