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CTCF regulates chromatin accessibility of the HBAD gene promoter during erythroid differentiation [UMI-4C]

ABSTRACT: Chromatin structure undergoes dynamic rearrangements during cell differentiation. The architectural protein CTCF plays diverse roles in this process. Here, we demonstrate that a subset of gene promoters alters their chromatin accessibility profiles upon CTCF binding during differentiation of the chicken erythroblast cell line HD3. Furthermore, we show that CTCF contributes to establishing a specific 3D chromatin architecture in the α-globin multigenic domain prior to differentiation in HD3 cells.

ORGANISM(S): Gallus gallus

PROVIDER: GSE296416 | GEO | 2026/04/29

REPOSITORIES: GEO

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CTCF regulates chromatin accessibility of the HBAD gene promoter during erythroid differentiation

Project description:Chromatin structure undergoes dynamic rearrangements during cell differentiation. The architectural protein CTCF plays diverse roles in this process. Here, we demonstrate that a subset of gene promoters alters their chromatin accessibility profiles upon CTCF binding during differentiation of the chicken erythroblast cell line HD3. Furthermore, we show that CTCF contributes to establishing a specific 3D chromatin architecture in the α-globin multigenic domain prior to differentiation in HD3 cells.

2026-04-29 | GSE296376 | GEO

CTCF regulates chromatin accessibility of the HBAD gene promoter during erythroid differentiation [ChIP-Seq]

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CTCF regulates chromatin accessibility of the HBAD gene promoter during erythroid differentiation [UMI-4C]

Project description:CTCF regulates chromatin accessibility of the HBAD gene promoter during erythroid differentiation [UMI-4C]

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Expression Profiling of Erythroid Progenitors After MYB shRNA Knockdown

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Expression Profiling of Erythroid Progenitors After MYB shRNA Knockdown

Project description:MYB plays a critical role as a regulator of erythropoieisis. We have shown that MYB silences epsilon and gamma-globin expression in erythroid progenitors. We here examine erythroid cells at the basophilic erythroblast stage of differentiation with MYB shRNA or control lentiviral transduction prior to differentiation. We have cultured CD34 cells and transduced the cells with lentiviruses harboring shRNAs targeting MYB or controls and then allowed the cells to differentiate down the erythroid lineage. At the basophilic erythroblast stage of differentiation, the cells were harvested and total RNA was extracted. This was used to hybridize to Affymetrix expression arrays using the HG-U133 Plus 2.0 platform to ascertain expression differences that occur with the knockdown of MYB.

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Project description:CTCF is an 11-zinc-finger DNA-binding protein that acts as a transcriptional repressor and insulator, as well as an architectural protein required for 3D genome folding. CTCF mediates long-range chromatin looping and is enriched at the boundaries of topologically associating domains (TADs), which are sub-megabase chromatin structures composed of genomic regions with high contact frequency. Although CTCF is essential for cycling cells and developing embryos, its in vitro removal has only modest effects over gene expression, challenging the generally accepted idea that TADs facilitate enhancer-promoter interactions within gene regulatory landscapes. However, the effects of an altered CTCF-mediated chromatin structure on gene regulation in vivo are poorly understood. Here, we have generated a ctcf knockout mutant in zebrafish that allows us to monitor the effect of CTCF loss of function during embryo patterning and organogenesis. CTCF absence leads to a loss of chromatin structure in zebrafish embryos and affects the expression of thousands of genes, among them many developmental genes. In addition, we show that chromatin accessibility, both at CTCF sites and at developmental cis-regulatory elements (CREs), is severely compromised in ctcf mutants. Probing chromatin interactions from developmental genes at high resolution, we further demonstrate that promoters fail to fully establish long-range contacts with their associated regulatory landscapes, leading to altered gene expression patterns during development. Therefore, our results demonstrate that CTCF and TADs are essential to finetune gene expression during embryonic development, providing the structural basis for the establishment of developmental gene regulatory landscapes.

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Project description:Mammalian genomes are subdivided into large (50-2000 kb) regions of chromatin referred to as Topologically Associating Domains (TADs or sub-TADs). Chromatin within an individual TAD contacts itself more frequently than with regions in surrounding TADs thereby directing enhancer-promoter interactions. In many cases, the borders of TADs are defined by convergently orientated boundary elements associated with CCCTC-binding factor (CTCF), which stabilises the cohesin complex on chromatin and prevents its translocation. This delimits chromatin loop extrusion which is thought to underlie the formation of TADs. However, not all CTCF-bound sites act as boundaries and, importantly, not all TADs are flanked by convergent CTCF sites. Here, we examined the CTCF binding sites within a ~70 kb sub-TAD containing the duplicated mouse α-like globin genes and their five enhancers (5’-R1-R2-R3-Rm-R4-α1-α2-3’). The 5’ border of this sub-TAD is defined by a pair of CTCF sites. Surprisingly, we show that deletion of the CTCF binding sites within and downstream of the α-globin locus leaves the sub-TAD largely intact. The predominant 3’ border of the sub-TAD is defined by a steep reduction in contacts: this corresponds to the transcribed α2-globin gene rather than the CTCF sites at the 3’-end of the sub-TAD. Of interest, the almost identical α1- and α2-globin genes interact differently with the enhancers, resulting in preferential expression of the proximal α1-globin gene which behaves as a partial boundary between the enhancers and the distal α2-globin gene. Together, these observations provide direct evidence that actively transcribed genes can behave as boundary elements.

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Characterisation of the mouse alpha-globin sub-TAD 3' boundary in erythroid cells [ChIP-seq]

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