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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

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.

2024-09-01 | GSE274928 | GEO

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

2024-09-01 | GSE275337 | GEO

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

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

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HIC2 represses BCL11A transcription to regulate hemoglobin switching during development (Capture-C)

Project description:The switch from fetal to adult hemoglobin production has been studied in great depth in part because of its relevance to the treatment of hemolobinopathies. Transcription factor BCL11A, which is essential for repression of the fetal beta-type globin (γ-globin) genes after birth, is largely controlled at the level of transcription but the mechanism of BCL11A developmental control is unknown. Here, using a CRISPR-Cas9 screen in human erythroblasts, we identify transcription factor HIC2 as a repressor of BCL11A transcription. HIC2 and BCL11A expression are anti-correlated in fetal and adult erythroblasts. Forced expression of HIC2 in adult erythroblasts silences BCL11A transcription and markedly induces γ-globin expression. HIC2 binds selectively to constituent erythroid developmental BCL11A enhancer to reduce chromatin accessibility and impair access by transcription factor GATA1, resulting in loss of enhancer activity and enhancer-promoter contacts. Conversely, loss of HIC2 in fetal erythroblasts increases enhancer accessibility, enables GATA1 binding and induces BCL11A transcription. HIC2 is unveiled as a critical evolutionarily conserved regulator of globin gene switching by imposing developmental control on the BCL11A gene.

2022-05-26 | GSE173583 | GEO

Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells (ChIP-seq)

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

| PRJNA725486 | ENA

Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells (ATAC-seq)

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

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HRI activates ATF4 to promote BCL11A transcription and fetal hemoglobin silencing [Capture-C]

Project description:Through a CRISPR-Cas9 guided loss-of-function screen in human erythroid cells we identified transcription factor ATF4, a known HRI-regulated protein, as a novel γ-globin repressor. ATF4 binds to a BCL11A enhancer to augment promoter contacts, stimulates BCL11A transcription to repress γ-globin expression. Notably, mice deficient for HRI displayed normal Bcl11a levels, suggesting species selective regulation that we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable. This illustrates potential limits of commonly used murine models of globin gene regulation.

2020-04-17 | GSE143962 | GEO

Let-7 miRNAs repress HIC2 to regulate BCL11A transcription and hemoglobin switching [Capture-C]

Project description:The fetal hemoglobin (HBG) regulator BCL11A is repressed by HIC2 to regulate hemoglobin switching. HIC2 itself is under developmental control, highly expressed in fetal tissues and decreased in adult cells, but the mechanism of this developmental regulation is unclear. Here, we demonstrate that HIC2 is developmentally controlled by miRNAs, and loss of global miRNA biogenesis through DICER1 depletion leads to upregulation of HIC2 and HBG. We subsequently identify the adult-expressed let-7 miRNA family as a repressor of HIC2 expression. Ectopic expression of let-7 in fetal-type cells repressed HIC2 levels, while let-7 inhibition in adult erythroblasts upregulated HIC2 levels. Let-7 regulates BCL11A and HBG through induction of HIC2 and reduction of GATA1 binding at the BCL11A erythroid enhancer. Finally, HIC2 depletion rescues BCL11A-mediated repression of fetal hemoglobin in let-7 inhibited cells. Together these data demonstrate a key miRNA-mediated mechanism for developmental regulation of BCL11A expression and fetal hemoglobin repression in adult erythroid cells.

2024-02-05 | GSE216194 | GEO

CAPTURE-3C-seq analysis of locus-specific long-range DNA interactions in HeLa stable cells expressing LAMPS and sgHS2

Project description:We demonstrate that LAMPS-mediated LLPS induces the formation of long-range chromatin interactions

2023-03-16 | GSE180547 | GEO