Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA317302 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3330050.fastq.gz | Fastqsanger.gz | |||
| SRR3330051.fastq.gz | Fastqsanger.gz | |||
| SRR3330044.fastq.gz | Fastqsanger.gz | |||
| SRR3330045.fastq.gz | Fastqsanger.gz | |||
| SRR3330046.fastq.gz | Fastqsanger.gz |
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Project description:Integrative analysis of 3D nucleome and chromatin accessibility reveals a chromatin barrier established for T-lineage commitment during early T cell development
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Project description:Hematopoiesis consists of step-wise commitment of multiple distinct intermediate differentiation stages before mature blood cells are generated1,2. Early progenitor cells have multiple cell fate potentials and retain plasticity to differentiate to alternative lineages, while later stages are fully committed to certain cell lineages and rarely alter their fates3,4. Although extensive studies have been performed on regulatory pathways in mature blood cells5-8, few have examined chromatin re-organization underlying the transcription programs in early progenitors of hematopoiesis. In particular, what roles chromatin organization plays in the cell fate commitment during the differentiation of early hematopoietic progenitor cells remains unclear. Here, we carried out an integrative analysis of 3D nucleome, chromatin accessibility and gene expression during early T cell development from hematopoietic stem cells (HSC) to CD4/CD8 double positive (DP) T cells. Analysis of these data sets revealed extensive A/B compartment flips and dynamic changes of chromatin accessibility at regulatory regions including promoters and enhancers during the development process. Remarkably, both the compartment flip and changes in chromatin accessibility display a monotonic pattern. While gradual and progressive changes in chromatin re-organization was observed at most development stages, an abrupt and striking genome-wide change in A/B compartment structure and chromatin accessibility occurred during the transition from double negative stage 2 (DN2) to DN3, which was accompanied with the loss of cell fate plasticity of DN3 to differentiate to alternative lineages, suggesting that a chromatin barrier is established at the DN3 stage to lock the cells in the T cell fate. The binding of PU.1, a key factor for the fate choice of early progenitor cells, and BCL11B, critically required for T cell commitment at late stages, was associated with increased long-distance interaction and chromatin accessibility and may coordinately contribute to the establishment of the 3D nucleome structure required for the lineage differentiation and commitment.
2018-02-20 | GSE79874 | GEO
Project description:Hematopoiesis consists of step-wise commitment of multiple distinct intermediate differentiation stages before mature blood cells are generated. Although extensive studies have been performed on regulatory pathways in mature blood cells, few have examined chromatin reorganization underlying the changes in transcription programs from early progenitors of hematopoiesis to mature immune cells. In particular, what roles chromatin organization plays in the cell fate commitment during the differentiation of early hematopoietic progenitor cells to committed T cells remains unclear. Here, we carried out an integrative analysis of 3D nucleome, chromatin accessibility and gene expression from hematopoietic stem cells (HSC) to CD4/CD8 double positive (DP) T cells. Analysis of these data sets revealed extensive reorganization of A/B compartments, topologically associating domains (TADs), and chromatin accessibility at transcriptional regulatory regions during the development process. Remarkably, all three levels of chromatin organization display a monotonic pattern of change. While gradual and progressive changes in chromatin reorganization was observed at most development stages, an abrupt genome-wide change in A/B compartment structure, TAD domain scores and chromatin accessibility occurred during the transition from double negative stage 2 (DN2) to DN3, which was accompanied with the loss of cell fate plasticity of DN3 to differentiate to alternative lineages, suggesting that a chromatin barrier is established at the DN3 stage to lock the cells in the T cell fate. This chromatin barrier may be reinforced by another genome-wide reorganization of chromatin at the DN4-to-DP transition. The binding of PU.1, a key factor for the fate choice of early progenitor cells, and BCL11B, critically required for T cell commitment at later stages, was associated with increased long-distance interaction and chromatin accessibility. Deletion of Bcl11b led to decreased chromatin interaction for BCL11B target genes, suggesting that it may contribute to the establishment of the 3D nucleome structure required for the lineage differentiation and commitment.
2018-02-20 | GSE79422 | GEO
Project description:Integrative analysis of 3D nucleome and chromatin accessibility reveals a chromatin barrier established for T-lineage commitment during early T cell development [Dnase-Seq, HiC-Seq, Mnase-Seq, RNA-Seq]
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Project description:Zfp260 choreographs the early stage lineage commitment of skeletal stem cells
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Project description:YY1 and CTCF Orchestrate a 3D Chromatin Looping Switch during Early Neural Lineage Commitment
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Project description:Interplays among lineage specific nuclear proteins, chromatin modifying enzymes and the basal transcription machinery govern cellular differentiation, but their dynamics of actions and coordination with transcriptional control are not fully understood. Alterations in chromatin structure appear to establish a permissive state for gene activation at some loci but they play an integral role in activation at other loci. To determine the predominant roles of chromatin states and factor occupancy in directing gene regulation during differentiation, we mapped chromatin accessibility, histone modifications, and nuclear factor occupancy genome-wide during mouse erythroid differentiation dependent on the master regulatory transcription factor GATA1. Remarkably, despite extensive changes in gene expression, the chromatin state profiles (proportions of a gene in a chromatin state dominated by activating or repressive histone modifications) and accessibility remain largely unchanged during GATA1-induced erythroid differentiation. In contrast, gene induction and repression are strongly associated with changes in patterns of transcription factor occupancy. Our results indicate that during erythroid differentiation, the broad features of chromatin states are established at the stage of lineage commitment, largely independently of GATA1. These determine permissiveness for expression, with subsequent induction or repression mediated by distinctive combinations of transcription factors. Using ChIP-Seq technology to examine DNase hypersensitivity, three transcription factors, and four histone modifications in Gata1-null murine G1E line and rescued G1E-ER4 subline, and also two of the transcription factors in mouse primary erythroblasts. ChIP input DNA was sequenced in each cell type as controls.
2011-07-05 | E-GEOD-30142 | biostudies-arrayexpress
Project description:Integrating transcription factor abundance with chromatin accessibility in human erythroid lineage commitment
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Project description:Tissue homeostasis and regeneration require activation and subsequent lineage commitment of tissue-resident stem cells (SCs). These state changes are controlled by epigenetic barriers. Using hair follicle stem cells (HFSCs) as paradigm, we studied how aging impacts the chromatin landscape and function of mammalian SCs. Analyses of genome-wide chromatin accessibility revealed that aged HFSCs displayed widespread reduction of chromatin accessibility specifically at key SC self-renewal and differentiation genes that were characterized by bivalent promoters carrying both activating and repressive chromatin marks. Consistently, aged HFSCs showed reduced self-renewing capacity and attenuated ability to activate expression of these bivalent genes upon regeneration. These functional defects were niche-dependent as transplantation of aged HFSCs into young recipients or into ex vivo niches restored SC functions and transcription of poised genes. Mechanistically, aged HFSC niche displayed wide-spread alterations in extracellular matrix composition and mechanics, resulting in compressive forces on SCs and subsequent transcriptional repression, leading to loss of bivalent promoters. Tuning tissue mechanics both in vivo and in vitro recapitulated age-related SC changes, implicating niche mechanics as a central regulator of genome organization and function leading to age-dependent SC exhaustion.
2021-05-07 | PXD018352 | Pride
Project description:Cell-lineage specification is a tightly regulated process that is dependent on appropriate expression of lineage- and developmental stage-specific transcriptional programs. Accessibility and inaccessibility of gene loci are controlled dynamically during cellular development. Here, we show that Chromodomain Helicase DNA-binding protein 4 (CHD4), a major ATPase/helicase subunit of Nucleosome Remodeling and Deacetylase Complexes (NuRD) in lymphocytes, is essential for specification of the early B cell lineage transcriptional program. In the absence of CHD4 in early B cell progenitors in vivo, B cell progenitors are arrested at an early pro-B-like stage of development, unresponsive to IL-7 receptor signaling and complete V(D)J rearrangements at Igh loci inefficiently. Importantly, CHD4-deficient B cells express a significant number of non-B cell lineage genes, including genes involved in the development of other hematopoietic lineages and neuronal cells. The absence of CHD4 increased chromatin accessibility at hundreds of these gene loci, suggesting that its ability to repress transcription by mobilizing nucleosomes and compacting chromatin is a barrier against inappropriate transcription. Together, our data demonstrate the importance of CHD4 in establishing and maintaining an appropriate transcriptome in early B lymphopoiesis via chromatin accessibility.
2019-04-30 | GSE123503 | GEO