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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner

ABSTRACT: Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner

PROVIDER: PRJNA869755 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21069620_1.fastq.gz	Fastqsanger.gz
	SRR21069620_2.fastq.gz	Fastqsanger.gz
	SRR21069621_1.fastq.gz	Fastqsanger.gz
	SRR21069621_2.fastq.gz	Fastqsanger.gz
	SRR21069622_1.fastq.gz	Fastqsanger.gz

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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [RNA-seq]

Project description:Erythroid genes having enhancers in a short distance appear to be transcriptionally activated by histone H3K27ac extension and intergenic transcription that are independent from TAL1.

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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [ChIP-seq]

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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [ChIP-seq]

Project description:Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [ChIP-seq]

| PRJNA869728 | ENA

Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [RNA-seq]

Project description:Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [RNA-seq]

| PRJNA869757 | ENA

Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:We used microarray profiling in erythroid cells to uncover TAL1 dependent genes in a hematopoietic differentiation context. Differentiated ex vivo hematopoietic multipotential progenitors isolated from adult peripheral blood. The knockdown of TAL1 (KD) was induced in pro-erythroblasts (Days 8 and 9 of differentiation) using lentivirus-delivered shRNA. A scramble (scr) shRNA sequence was used as a negative control.

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TAL1 knock down in human erythroid progenitors

Project description:We used microarray profiling in erythroid cells to uncover TAL1 dependent genes in a hematopoietic differentiation context.

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Genome-wide maps of Scl/TAL1 in human erythroid cells.

Project description:ChIP-Seq experiments using an Scl/TAL1 antibody were carried out in primary erythroid cells cultured from two individuals of Caucasian origin. ChIP-Seq libraries were prepared from two biological replicates for each individual. ChIP DNA was processed for Illumina High-throughput sequencing according to Illumina protocol. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA from each experiments, we generated a high-resolution map of Scl/TAL1 genomic targets in human erythroid cells. We find that WGATAR and the combinatorial CTG(n9)GATA are the most significant motifs responsible for the chromatin occupancy by Scl/TAL1. In addition, other motifs are also significantly enriched at the Scl/TAL1 targets. Amongst these were binding sites for known TFs (Sp/XKLF, RUNX1, NFE2). We next investigated how many of these targets varied between these two individuals. We find that 0.8% of Scl/TAL1 binding regions differ significantly between the two individuals.

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Project description:A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes for six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.

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