Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA285264 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2043932.fastq.gz | Fastqsanger.gz | |||
| SRR2043934.fastq.gz | Fastqsanger.gz | |||
| SRR2043935.fastq.gz | Fastqsanger.gz | |||
| SRR2043936.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
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Project description:The modulation of chromatin structure is a key step in transcription regulation in eukaryotic cells. Mammalian erythropoiesis is accompanied by dynamic alterations in chromatin structure and gene expression, but the epigenetic regulators that modulate and coordinate these changes are largely unknown. USF, Setd1a and NURF complexes interact to regulate chromatin architecture in erythropoiesis, but the basis for this regulation is unknown. We studied this process using both murine and human models of erythropoiesis. In human primary erythroid cells, H3K4me3, USF1/2, and BPTF, a component of the NURF complex, were significantly co-enriched at more than 50% of transcription start sites (TSSs) of erythroid genes, associated with repositioning of promoter- or enhancer-associated nucleosomes. Depletion of Setd1a, an H3K4 trimethylase, led to a reduction of promoter-associated H3K4 methylation, inhibition of gene transcription and blockade of erythroid differentiation. This was associated with alterations in NURF complex-mediated nucleosome repositioning at erythroid gene promoters and chromatin accessibility. Setd1a deficiency caused decreased associations between the LCR and the -major globin promoter as well as reduced expression of the adult β-globin gene. In vivo, mice deficient for Setd1a in the erythroid compartment resulted in reduced Ter119/CD71 positive bone marrow erythroblasts, peripheral blood RBCs, and hemoglobin levels. These data indicate that Setd1a and NURF complexes coordinately regulate erythroid promoter chromatin dynamics during erythroid differentiation.
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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.
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Project description:The Cohesin complex critically controls interactions between proximal and distal cis-regulatory elements, while Cohesin disruption causes improper gene activation. This process associates with biased hematopoiesis, and Cohesin mutations are common in myeloid neoplasia. In this study, we initially explore Cohesin-associated dynamics and regulation of hematopoietic stem cell renewal and erythropoiesis. Cohesin binding to chromatin increases during erythroid differentiation at active promoters and enhancers only, with pre-binding of Etv6 predicting the subsequent dynamics of Cohesin binding at these elements. Etv6 also binds with the Cohesin complex at chromatin during haematopoiesis. Perturbation of Cohesin members does not alter hematopoietic self-renewal, but severely impairs erythroid differentiation. As in normal erythroid differentiation, the strongest impairment of gene activation in Cohesin-perturbed erythropoiesis occurs at Etv6-pre-bound loci. Taken together these findings propose a mechanism for how the Cohesin complex regulates the induction of gene expression during differentiation and how this may be perturbed in myeloid malignancies.
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