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

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

PROVIDER: PRJNA869728 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21068083_1.fastq.gz	Fastqsanger.gz
	SRR21068083_2.fastq.gz	Fastqsanger.gz
	SRR21068084_1.fastq.gz	Fastqsanger.gz
	SRR21068084_2.fastq.gz	Fastqsanger.gz
	SRR21068085_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 [ChIP-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 [RNA-seq]

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

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

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

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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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The transcription factor TAL1 and the miR-17-92 cluster establish a regulatory loop

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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Project description:Aberrant activation of the TAL1 oncogene is associated with up to 60% of T-ALL patients and is involved in CTCF mediated genome organization within the TAL1 locus, suggesting the importance of the CTCF boundary in the molecular pathogenesis of T-ALL. Here, we show that deletion of CTCF binding site (CBS) or alternation of CTCF boundary orientation alters expression of the TAL1 oncogene in a cell context dependent manner. Deletion of the CTCF binding site located at -31 Kb upstream of TAL1 (-31CBS) reduces chromatin accessibility in the +51 enhancer and the TAL1 promoter I, and blocks long-range interaction between the +51 erythroid enhancer and TAL1 promoter 1b that inhibits expression of TAL1 in erythroid cells, but not in T-ALL cells. However, in the TAL1 expressed T-ALL primary patient samples or cell line, the T-ALL prone TAL1 promoter IV specifically interacts with the +19 stem cell enhancer that is located 19 kb downstream of the TAL1 promoter and required for TAL1 transcription in the hematopoietic stem cell (HSC) stage. Inversion of -31CBS orientation, but not deletion of -31CBS, alters chromatin accessibility, enhancer/promoter histone modifications, CTCF-mediated topological associated domain (TAD), and enhancer/promoter interaction in the TAL1 locus leading to inhibition of TAL1 oncogene expression and TAL1-driven T cell leukemogenesis. Thus, our data reveal that the TAL1 +19 stem cell enhancer acts not only as stem cell enhancer, but also as a leukemia specific enhancer to activate the TAL1 oncogene in T-ALL. Manipulation of CTCF defined chromatin boundary can alter TAL1 TAD and oncogenic transcription networks in leukemogenesis.

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