Chromatin accessibility analysis of adipose progenitors (AP).
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA487081 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7733570_1.fastq.gz | Fastqsanger.gz | |||
| SRR7733570_2.fastq.gz | Fastqsanger.gz | |||
| SRR7733571_1.fastq.gz | Fastqsanger.gz | |||
| SRR7733571_2.fastq.gz | Fastqsanger.gz | |||
| SRR7733572_1.fastq.gz | Fastqsanger.gz |
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Project description:We hypothesized that core transcriptional regulatory circuitries analysis could be used in conjunction with gene expression profiling data to nominate specific TFs for additional functional studies of AP cell state. To accomplish this analysis, we utilized the assay of transposase-accessible chromatin coupled to massively parallel sequencing (ATAC-seq) to identify putative enhancers in APs. The AP preparation involved adipose tissue digestion, and negative selection of the stromal vascular fraction (depletion of CD31+ endothelial cells and Lineage positive cells).
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Project description:Comparision of gene expression in adipose progenitors(AP) relative to adipose tissue(AT)
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Project description:<p>Non-coding regions comprise most of the human genome and harbor a significant fraction of risk alleles for neuropsychiatric diseases, yet their functions remain poorly defined. We created a high-resolution map of non-coding elements involved in human cortical neurogenesis by contrasting chromatin accessibility and gene expression in the germinal zone and cortical plate of the developing cerebral cortex. To obtain a high resolution depiction of chromatin structure and gene expression in developing human fetal cortex, we dissected the post-conception week (PCW) 15-17 human neocortex into two major anatomical divisions to distinguish between proliferating neural progenitors and post mitotic neurons: (1) GZ: the neural progenitor-enriched region encompassing the ventricular zone (VZ), subventricular zone (SVZ), and intermediate zone (IZ) and (2) CP: the neuron-enriched region containing the subplate (SP), cortical plate (CP), and marginal zone (MZ). Tissues were obtained from three independent donors and three to four technical replicates from each tissue were processed for ATAC-seq to define the landscape of accessible chromatin and RNA-seq for genome-wide gene expression profiling.</p>
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Project description:The zebrafish has emerged as a powerful model to study cardiac regeneration; however, the mechanisms by which cardiomyocytes respond to damage by disassembling sarcomeres, proliferating, and repopulating the injured area remain unclear. Here, we show that AP-1 transcription factors play an essential role in regulating the cardiomyocyte response. Using ATAC-Seq, we first find that the cardiomyocyte chromatin accessibility landscape is dynamic following cryoinjury, and that AP-1 motifs are the most highly enriched in regions that gain accessibility during regeneration. Using a cardiomyocyte-specific dominant-negative approach, we show that AP-1 promotes cardiomyocyte proliferation as well as chromatin accessibility at genes regulating sarcomere disassembly and cardiomyocyte protrusion into the injured area. We further find distinct temporal requirements for AP-1 during cardiac regeneration. Altogether, these results indicate that AP-1 plays a key role in the cardiomyocyte response to injury by promoting chromatin accessibility changes, allowing the activation of gene expression programs that support regeneration.
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Project description:The project aims to identify differentially expressed genes in adipose progenitors that were freshly isolated from wild-type or Nr4a1-/- mice. The AP preparation involved adipose tissue digestion, and negative selection of the stromal vascular fraction (depletion of CD31+ endothelial cells and Lineage positive cells.
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Project description:The increased stiffness of the extracellular matrix is a key driver of liver fibrosis. The activated hepatic stellate cell (HSC) is the major producer of extracellular matrix (ECM) components. While little is known about the epigenomic changes that underlie the fibrogenic impact of ECM mechanics. In this study, we utilized a reliable in vitro system to mimic liver cirrhosis and integrated multi-omics analysis, which includes time-series RNA-seq and ATAC-seq as well as histone modification Cut&Tag, with imaging and biochemical essays to study the mechanism underlying the biomechanics function on fibrotic phenotype. We found that cells cultured in stiff matrix displayed more accessible chromatin sites, consisting of amount regions became accessible before stable fibrotic phenotype. We defined these regions as primed chromatin that chromatin accessibility foreshadows changes in gene expression. This kind of chromatin enriched in cytoskeleton organization and responding to mechanical stimulus biological process. Here, we depicted the AP-1 transcription factor family as being responsible for driving the construction of primed chromatin. Among AP-1 transcription factors, we confirmed JUN was critical to reconstruct chromatin accessibility to promote fibrogenic genotype. In addition, we described ERK contribute to the activation of JUN resulting in its binding on chromatin. Our results profiled a dynamic landscape of chromatin accessibility and defined the primed chromatin that contribute to fibrosis during responding to stiff matrix. We identified that AP-1 was capable of reorganizing the chromatin accessibility in mechanotransduction.
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Project description:The increased stiffness of the extracellular matrix is a key driver of liver fibrosis. The activated hepatic stellate cell (HSC) is the major producer of extracellular matrix (ECM) components. While little is known about the epigenomic changes that underlie the fibrogenic impact of ECM mechanics. In this study, we utilized a reliable in vitro system to mimic liver cirrhosis and integrated multi-omics analysis, which includes time-series RNA-seq and ATAC-seq as well as histone modification Cut&Tag, with imaging and biochemical essays to study the mechanism underlying the biomechanics function on fibrotic phenotype. We found that cells cultured in stiff matrix displayed more accessible chromatin sites, consisting of amount regions became accessible before stable fibrotic phenotype. We defined these regions as primed chromatin that chromatin accessibility foreshadows changes in gene expression. This kind of chromatin enriched in cytoskeleton organization and responding to mechanical stimulus biological process. Here, we depicted the AP-1 transcription factor family as being responsible for driving the construction of primed chromatin. Among AP-1 transcription factors, we confirmed JUN was critical to reconstruct chromatin accessibility to promote fibrogenic genotype. In addition, we described ERK contribute to the activation of JUN resulting in its binding on chromatin. Our results profiled a dynamic landscape of chromatin accessibility and defined the primed chromatin that contribute to fibrosis during responding to stiff matrix. We identified that AP-1 was capable of reorganizing the chromatin accessibility in mechanotransduction.
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