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Analysis of chromatin occupancy in erythroid cells by CUT&RUN following CRISPR editing of BCL11A enhancer

ABSTRACT: The mechanisms underlying the remarkable efficacy of CRISPR-mediated BCL11A enhancer ablation remain poorly understood. Here, we employ CUT&RUN to investigate active and repressive histone modifications, as well as cohesin and CTCF binding, to uncover epigenetic changes under various editing conditions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE292753 | GEO | 2025/11/13

REPOSITORIES: GEO

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Analysis of chromatin occupancy in erythroid cells by CUT&Tag following CRISPR editing of BCL11A enhancer

Project description:The mechanisms underlying the remarkable efficacy of CRISPR-mediated enhancer ablation remain poorly understood. Here, we employ CUT&Tag to investigate histone modifications following BCL11A enhancer editing or CTCF disruption.

2025-11-13 | GSE292695 | GEO

Analysis of chromatin accessbility in erythroid cells following CRISPR editing or ASO perturbation of BCL11A enhancer

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 | GSE292669 | GEO

Analysis of chromatin occupancy in erythroid cells by CUT&RUN following CRISPR editing of BCL11A enhancer

Project description:Analysis of chromatin occupancy in erythroid cells by CUT&RUN following CRISPR editing of BCL11A enhancer

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Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells

Project description:Reactivation of fetal hemoglobin expression by down-regulation of BCL11A is a promising treatment of -hemoglobinopathies. A detailed understanding of BCL11A-mediated repression of -globin gene (HBG1/2) transcription is lacking, as studies to date used perturbations by shRNA or CRISPR/Cas9 gene editing. We leveraged the dTAG PROTAC platform to acutely deplete BCL11A protein in erythroid cells and examined consequences by PRO-seq, proteomics, chromatin accessibility, and histone profiling. Among ≤ 31 genes repressed by BCL11A, HBG1/2 and HBZ show the most abundant and progressive changes in transcription and chromatin accessibility upon BCL11A loss. Transcriptional changes at HBG1/2 were detected in < 2h. Robust HBG1/2 reactivation upon acute BCL11A-depletion occurred without loss of promoter 5methylcytosine (5mC). Using targeted protein degradation, we establish a hierarchy of gene reactivation at BCL11A targets, in which nascent transcription is followed by increased chromatin accessibility, and both are uncoupled from promoter DNA methylation at the HBG1/2 loci.

2023-10-24 | PXD030307 | Pride

Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells

2022-07-27 | PXD030301 | Pride

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

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BCL11A is required for normal erythropoiesis [CUT&Run]

Project description:BCL11A is required for normal erythropoiesis [CUT&Run]

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Human CD34-derived erythroid progenitors treated with BCL11A siRNAs

2008-12-05 | GSE13284 | GEO

Expression data from BCL11A-null and wild-type bone marrow erythroid pregenitors

Project description:BCL11A is a critical mediator of hemoglobin switching and gamma-globin silencing. In this study, we showed the BCL11A is required in vivo for developmental silencing of gamma-globin genes in adult animals. We used microarray to determine the changes in gene expression profile after loss of BCL11A in adult erythroid cells CD71+Ter119+ erythroid progenitor cells were FACS-sorted from bone marrows of 6-week old control (Bcl11a +/+) and BCL11A knockout (Bcl11a fl/fl EpoR-Cre+) mice.

2012-03-22 | E-GEOD-28333 | biostudies-arrayexpress

RNAi profiling by array of human CD34-derived erythroid progenitors treated with BCL11A siRNAs

Project description:Differences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here we examine BCL11A as a potential regulator of HbF expression. The high HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a therapeutic target for reactivation of HbF in beta-hemoglobin disorders. BCL11A siRNA label: B, NT siRNA label: N Experiment Overall Design: Microarray expression analysis from CD34-derived erythroid progenitors treated with either non-targeting (NT) control siRNAs or BCL11A targeting siRNAs. Six samples from the NT control and six samples from the BCL11A siRNA treatment are included. Cells were harvested on day 7 of erythroid differentiation after introduction of siRNAs on day 0 of the differentiation protocol. Experiment Overall Design: 6 BCL11A siRNA datasets, 6 control (NT) datasets

2009-01-13 | E-GEOD-13284 | biostudies-arrayexpress

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