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Analysis of locus-specific long-range chromatin interactions in BCL11A WT and KO HUDEP-2 cells by CAPTURE

ABSTRACT: Analysis of locus-specific long-range chromatin interactions in BCL11A WT and KO HUDEP-2 cells by CAPTURE

PROVIDER: PRJNA750797 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15300862_1.fastq.gz	Fastqsanger.gz
	SRR15300862_2.fastq.gz	Fastqsanger.gz
	SRR15300863_1.fastq.gz	Fastqsanger.gz
	SRR15300863_2.fastq.gz	Fastqsanger.gz
	SRR15300864_1.fastq.gz	Fastqsanger.gz

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Analysis of locus-specific long-range chromatin interactions in BCL11A WT and KO HUDEP-2 cells by CAPTURE

Project description:We determined the locus-specific long-range chromatin interactions associated with the human beta-globin gene cluster in BCL11A wild-type and knockout HUDEP-2 cells

2021-07-30 | GSE181151 | GEO

Analysis of CTCF-mediated chromatin interactions at the BCL11A locus in HUDEP-2 cells by Micro-Capture-C (MCC)

Project description:Three-dimensional chromatin structures, including promoter-enhancer interactions and CTCF looping, are essential for gene regulation. In this study, we apply Micro-Capture-C (MCC) to analyze chromatin structures at the BCL11A locus.

2025-11-13 | GSE292671 | GEO

Analysis of chromatin structure of the BCL11A locus in HUDEP-2 cells by Capture-Pore-C (CPC)

Project description:CRISPR editing of an intronic enhancer within the BCL11A gene reactivates fetal hemoglobin (HbF) in adult erythroid cells, serving as a gene-based therapy for hemoglobinopathies. However, the mechanisms underlying the remarkable efficacy of CRISPR-mediated enhancer ablation remain poorly understood. We describe an evolutionarily conserved, enhancer-dependent chromatin architecture, the enhancer-CTCF rosette, essential for chromatin insulation and the developmental expression of BCL11A in hematopoiesis. CRISPR-mediated disruption of lineage-specific BCL11A enhancers impairs enhancer RNA transcription and NIPBL-cohesin loading, leading to destabilized chromatin configuration, impaired chromatin insulation, and epigenetic silencing of BCL11A. Antisense oligonucleotide-mediated depletion of enhancer RNA silences BCL11A by disrupting chromatin insulation in adult erythroid cells.

2025-11-13 | GSE292694 | GEO

Analysis of CTCF-mediated chromatin interactions at the BCL11A locus in HUDEP-2 cells by Micro-Capture-C (MCC)

Project description:Analysis of CTCF-mediated chromatin interactions at the BCL11A locus in HUDEP-2 cells by Micro-Capture-C (MCC)

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Analysis of nascent transcription by PRO-seq in HUDEP-2 cells following CRISPR editing of BCL11A enhancer

2025-11-13 | GSE292697 | GEO

Analysis of chromatin structure of the BCL11A locus in HUDEP-2 cells by Capture-Pore-C (CPC)

Project description:Analysis of chromatin structure of the BCL11A locus in HUDEP-2 cells by Capture-Pore-C (CPC)

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Analysis of nascent transcription by EU-seq in HUDEP-2 cells following CTCF degredation

Project description:CTCF plays a crucial role in looping and insulation, yet its role in BCL11A regulation remains unclear. Here, we utilize EU-seq to measure nascent transcription in HUDEP-2 cells with CTCF-AID.

2025-11-13 | GSE292670 | GEO

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent

Project description:Prior evidence indicates that the erythroid cellular response to glucocorticoids (GC) has developmental specificity, namely, that developmentally more advanced cells that are undergoing or have undergone fetal to adult globin switching are more responsive to GC-induced expansion. To investigate the molecular underpinnings of this, we focused on the major developmental globin regulator BCL11A. We compared: a) levels of expression and nuclear content of BCL11A in adult erythroid cells upon GC stimulation; b) response to GC of CD34+ cells from patients with BCL11A microdeletions and reduced BCL11A expression, and; c) response to GC of two cellular models (HUDEP-2 and adult CD34+ cells) before and after reduction of BCL11A expression by shRNA. We observed that: a) GC-expanded erythroid cells from a large cohort of blood donors displayed amplified expression and nuclear accumulation of BCL11A; b) CD34+ cells from BCL11A microdeletion patients generated fewer erythroid cells when cultured with GC compared to their parents, while the erythroid expansion of the patients was similar to that of their parents in cultures without GC, and; c) adult CD34+ cells and HUDEP-2 cells with shRNA-depleted expression of BCL11A exhibit reduced expansion in response to GC. In addition, RNA-seq profiling of shRNA-BCL11A CD34+ cells cultured with and without GC was similar (very few differentially expressed genes), while GC-specific responses (differential expression of GILZ and of numerous additional genes) were observed only in controls cells with unperturbed BCL11A expression. These data indicate that BCL11A is an important participant of certain aspects of the stress pathway sustained by GC.

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The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent, microdeletion patients.

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Project description:Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells

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