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Cohesin loading at regulatory elements shapes 3D genome folding during erythropoiesis

ABSTRACT: During erythropoiesis, differentiating cells silence much of the genome while maintaining high expression of select genes. It remains unclear whether this transcriptional specialization is linked to specific changes in 3D genome organization. We generated deep Micro-C maps across human erythropoiesis to understand the relationship between cis-regulatory elements and cohesin-mediated loop extrusion during erythroid differentiation. Shifts in erythroid 3D genome structure during differentiation and under perturbations of transcription factors and cohesin subunits/cofactors indicates that a subset of CREs concentrate loop extrusion near key genes during erythroid differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE341414 | GEO | 2026/07/31

REPOSITORIES: GEO

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Cohesin loading at regulatory elements shapes 3D genome folding during erythropoiesis [RNA-Seq]

Project description:During erythropoiesis, differentiating cells silence much of the genome while maintaining high expression of select genes. It remains unclear whether this transcriptional specialization is linked to specific changes in 3D genome organization. We generated deep Micro-C maps across human erythropoiesis to understand the relationship between cis-regulatory elements and cohesin-mediated loop extrusion during erythroid differentiation. Shifts in erythroid 3D genome structure during differentiation and under perturbations of transcription factors and cohesin subunits/cofactors indicates that a subset of CREs concentrate loop extrusion near key genes during erythroid differentiation.

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Loop extrusion by cohesin plays a role in enhancer-activated gene expression early in differentiation (NG Capture-C)

Project description:Enhancers and their target promoters often come into close physical proximity when activated. This may be explained by a variety of mechanisms, including cohesin-mediated chromatin loop extrusion. However, acute depletion of cohesin does not cause widespread changes in gene expression. We have tested the role of cohesin-mediated loop extrusion in gene expression at the mouse alpha-globin locus during erythropoiesis. Acute depletion of cohesin disrupts alpha-globin expression at early but not late stages of differentiation. Furthermore, when single or multiple CTCF sites, known to block cohesin, are placed between the alpha-globin enhancers and promoters, alpha-gene expression is disrupted. Importantly, the CTCF site’s orientation is critical, suggesting that within this activated domain, in definitive erythroid cells cohesin predominantly but not exclusively, translocates from the enhancers to the promoters. We find that loop extrusion does play an important role in establishing enhancer-promoter proximity and consequent expression of inducible genes during differentiation.

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Project description:CTCF structures 3D genome folding by anchoring or forestalling cohesin loop extrusion, but the exact mechanism remains obscure. Here, using clustered protocadherins (cPcdh) as model genes, we report that CTCF stabilizes or facilitates cohesin loop extrusion by enhancing its processivity. Specifically, we show that, compared with the Pcdh alpha and gamma clusters, the Pcdh beta cluster is greatly affected upon CTCFY226A/F228A mutation in the N-terminal domain. Given the long-range distance of the Pcdh beta cluster from the distal enhancer, this finding has interesting implications in CTCF regulation of cohesin processivity along the linear chromatin during DNA loop extrusion. In particular, the effect on cohesin processivity upon CTCFY226A/F228A mutation is conspicuously similar to that of WAPL overexpression, demonstrating that, contrary to the general view of blocking or forestalling cohesin, CTCF actually enhances or facilitates cohesin loop extrusion.

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CCCTC-binding Factor N-terminal Domain Regulates Clustered Protocadherin Gene Expression by Enhancing Cohesin Processivity

Project description:CTCF (CCCTC-binding factor) instructs 3D genome folding by anchoring or forestalling cohesin loop extrusion, but the exact mechanism remains obscure. Here, using clustered protocadherins (cPcdh) as model genes, we report that CTCF assists or facilitates cohesin loop extrusion by enhancing its processivity. Specifically, we show that, compared with the Pcdh alpha and gamma clusters, the Pcdh beta cluster is greatly affected upon CTCF Y226A/F228A mutation in the N-terminal domain. Given the long-range distance of the Pcdh beta cluster from the distal enhancer, this finding has interesting implications in CTCF regulation of cohesin processivity along the linear chromatin during DNA loop extrusion. In particular, the effect on cohesin processivity upon CTCF Y226A/F228A mutation is conspicuously similar to that of WAPL overexpression, suggesting that, in addition to the general view of blocking or forestalling cohesin, CTCF may also enhances or facilitates cohesin loop extrusion.

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