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CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (ChIP-Seq)

ABSTRACT: ChIP-Seq analysis of CTCF enrichment in WT hiPSCs and hiPSCs with CTCF deletion

ORGANISM(S): Homo sapiens

PROVIDER: GSE247425 | GEO | 2023/11/24

REPOSITORIES: GEO

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CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs.

Project description:Pluripotent stem cells are characterized by their differentiation potential toward endoderm, mesoderm, and ectoderm. However, it is still largely unclear how these cell-fate decisions are mediated by epigenetic mechanisms. In this study, we explored the relevance of CCCTC-binding factor (CTCF), a zinc finger-containing DNA-binding protein, which mediates long-range chromatin organization, for directed cell-fate determination. We generated human induced pluripotent stem cell (iPSC) lines with deletions in the protein-coding region in exon 3 of CTCF, resulting in shorter transcripts and overall reduced protein expression. Chromatin immunoprecipitation showed a considerable loss of CTCF binding to target sites. The CTCF deletions resulted in slower growth and modest global changes in gene expression, with downregulation of a subset of pluripotency-associated genes and neuroectodermal genes. CTCF deletion also evoked DNA methylation changes, which were moderately associated with differential gene expression. Notably, CTCF-deletions lead to upregulation of endo-mesodermal associated marker genes and epigenetic signatures, whereas ectodermal differentiation was defective. These results indicate that CTCF plays an important role in the maintenance of pluripotency and differentiation, especially towards ectodermal lineages.

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CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (methylation)

Project description:Pluripotent stem cells are characterized by their differentiation potential toward endoderm, mesoderm, and ectoderm. However, it is still largely unclear how these cell-fate decisions are mediated by epigenetic mechanisms. In this study, we explored the relevance of CCCTC-binding factor (CTCF), a zinc finger-containing DNA-binding protein, which mediates long-range chromatin organization, for directed cell-fate determination. We generated human induced pluripotent stem cell (iPSC) lines with deletions in the protein-coding region in exon 3 of CTCF, resulting in overall reduced expression and shorter transcripts. These lines showed a considerable loss of CTCF binding to target sites. The CTCF deletions resulted in slower growth and modest global changes in gene expression, with down-regulation of a subset of pluripotency-associated genes and neuroectodermal genes. CTCF deletion also evoked DNA methylation changes, which were moderately associated with differential gene expression. Notably, CTCF-deletions lead to up-regulation of endo-mesodermal associated marker genes and epigenetic signatures, whereas ectodermal differentiation was defective. These results indicate that CTCF plays an important role in the maintenance of pluripotency and differentiation, especially towards ectodermal lineages.

2023-11-24 | GSE247427 | GEO

CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (RNA-Seq)

Project description:Pluripotent stem cells are characterized by their differentiation potential toward endoderm, mesoderm, and ectoderm. However, it is still largely unclear how these cell-fate decisions are mediated by epigenetic mechanisms. In this study, we explored the relevance of CCCTC-binding factor (CTCF), a zinc finger-containing DNA-binding protein, which mediates long-range chromatin organization, for directed cell-fate determination. We generated human induced pluripotent stem cell (iPSC) lines with deletions in the protein-coding region in exon 3 of CTCF, resulting in overall reduced expression and shorter transcripts. These lines showed a considerable loss of CTCF binding to target sites. The CTCF deletions resulted in slower growth and modest global changes in gene expression, with down-regulation of a subset of pluripotency-associated genes and neuroectodermal genes. CTCF deletion also evoked DNA methylation changes, which were moderately associated with differential gene expression. Notably, CTCF-deletions lead to up-regulation of endo-mesodermal associated marker genes and epigenetic signatures, whereas ectodermal differentiation was defective. These results indicate that CTCF plays an important role in the maintenance of pluripotency and differentiation, especially towards ectodermal lineages.

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CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (methylation)

Project description:CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (methylation)

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CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs

Project description:CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs

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CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-24 | GSE247428 | GEO

CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (RNA-Seq)

Project description:CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (RNA-Seq)

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CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (ChIP-Seq)

Project description:CTCF deletion alters the pluripotency and DNA methylation profile of human iPSCs (ChIP-Seq)

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ZNF143 deletion alters enhancer/promoter looping and CTCF/cohesin geometry [HiChIP]

Project description:The transcription factor ZNF143 contains seven tandem zinc fingers and is involved in 3D genome construction; however, the mechanism by which ZNF143 functions in chromatin looping remains unclear. Here, we show that ZNF143 directionally recognizes diverse genomic sites and is required for chromatin looping between these sites. In addition, ZNF143 is located between CTCF and cohesin at numerous CTCF sites and ZNF143 removal narrows the space between CTCF and cohesin. Moreover, genetic deletion of ZNF143, in conjunction with acute CTCF depletion, revealed that ZNF143 and CTCF collaborate to regulate higher-order genome organization. Thus, ZNF143 is recruited by CTCF to the CTCF sites to regulate TAD formation and genome compartmentalization whereas directional recognition of DNA motifs directly by ZNF143 itself regulates promoter activity via chromatin looping.

2023-11-07 | GSE236635 | GEO