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Noncoding RNA, ncRNA-a3, epigenetically regulates TAL1 transcriptional program during erythropoiesis (NG Capture-C)

ABSTRACT: Noncoding RNA, ncRNA-a3, epigenetically regulates TAL1 transcriptional program during erythropoiesis (NG Capture-C)

PROVIDER: PRJNA1136481 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29845777_1.fastq.gz	Fastqsanger.gz
	SRR29845777_2.fastq.gz	Fastqsanger.gz
	SRR29845778_1.fastq.gz	Fastqsanger.gz
	SRR29845778_2.fastq.gz	Fastqsanger.gz
	SRR29845779_1.fastq.gz	Fastqsanger.gz

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Noncoding RNA, ncRNA-a3, epigenetically regulates TAL1 transcriptional program during erythropoiesis (NG Capture-C)

Project description:Here, we showed that a long non-coding RNA (lncRNA), ncRNA-a3 that is transcribed from TAL1 erythroid +51kb enhancer, is required for TAL1 activation during EPO-induced lineage commitment and formation of erythroblasts. ncRNA-a3 regulates long-range chromatin interactions between +51 enhancer, promoter and other regulatory elements in the TAL1 locus to maintain the erythroid interaction hub. By binding and recruiting p300/BRG1 to the TAL1 locus ncRNA-a3 facilitates chromatin accessibility in the TAL1 locus and activates TAL1 transcription program, including subsequent epigenetic and transcriptional activation of erythroid specific TAL1 target genes.

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Noncoding RNA, ncRNA-a3, epigenetically regulates TAL1 transcriptional program during erythropoiesis (RNA-Seq)

Project description:Noncoding RNA, ncRNA-a3, epigenetically regulates TAL1 transcriptional program during erythropoiesis (RNA-Seq)

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Project description:Noncoding RNA, ncRNA-a3, epigenetically regulates TAL1 transcriptional program during erythropoiesis (ATAC-Seq)

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Project description:Noncoding RNA, ncRNA-a3, epigenetically regulates TAL1 transcriptional program during erythropoiesis (CUT&Run)

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Hematopoiesis and cell growth are differentially regulated by TAL1 isoforms

Project description:T-cell acute lymphoblastic leukemia (T-ALL) protein 1 (TAL1) is a central transcription factor in hematopoiesis. The timing and level of TAL1 expression orchestrate the differentiation to specialized blood cells and its overexpression is the most common cause of T-ALL. Here we studied the two protein isoforms of TAL1, short and long, that are generated by the use of alternative promoters as well as by alternative splicing. We analyzed the expression of each isoform by deleting an enhancer or insulator, or by opening chromatin at the enhancer location. Our results show that each enhancer promotes expression from a specific TAL1 promoter. Expression from a specific promoter gives rise to a unique 5’ UTR with differential regulation of translation. In addition, the enhancers regulate TAL1 exon 3 alternative splicing by altering the chromatin at its location. Furthermore, our results indicate that TAL1-short binds more strongly to TAL1 E-protein partners and function as a stronger transcription factor than TAL1-long. Specifically TAL1-short has a unique transcription signature promoting apoptosis. Finally, expressing both isoforms in mice bone marrow, we found that while overexpression of both isoforms prevents lymphoid differentiation, expression of TAL-short alone reduced survival capability of hematopoietic stem cells. Furthermore, we found that TAL1-short promoted erythropoiesis and reduced cell survival in the AML cell line K562. While TAL1 and its partners are considered promising therapeutic targets in the treatment of T-ALL, our results show that TAL1-short could act as a tumor suppressor and suggest that altering TAL1 isoform’s ratio could be a preferred therapeutic approach.

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