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KLF4 inhibits early neural differentiation of ESCs by coordinating specific 3D chromatin structure

ABSTRACT: KLF4 inhibits early neural differentiation of ESCs by coordinating specific 3D chromatin structure

PROVIDER: PRJNA798967 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17681132.fastq.gz	Fastqsanger.gz
	SRR17681133_1.fastq.gz	Fastqsanger.gz
	SRR17681133_2.fastq.gz	Fastqsanger.gz
	SRR17681134_1.fastq.gz	Fastqsanger.gz
	SRR17681134_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

KLF4 inhibits early neural differentiation of ESCs by coordinating specific 3D chromatin structure

Project description:Neural differentiation of embryonic stem cells (ESCs) requires precisely orchestrated gene regulation, a process governed in part by changes in 3D chromatin structure. How these changes regulate gene expression in this context remains unclear. In this study, we observed enrichment of the transcription factor KLF4 at some poised or closed enhancers at TSS-linked regions of genes associated with neural differentiation, such as Pax6. Combination analysis employing ChIP, HiChIP and RNA-seq data indicated that KLF4 loss in ESCs induced changes in 3D chromatin structure, including increased chromatin interaction loops between neural differentiation-associated genes and active enhancers. And changes of chromatin structure upregulated expression of neural differentiation-associated genes and promoted early neural differentiation. This study reveals that KLF4 has a differentiation inhibitory effect in regulating 3D chromatin structure and suggests KLF4 inhibits early neural differentiation by regulation of 3D chromatin structure, which is a new mechanism of early neural differentiation.

2022-06-01 | GSE194068 | GEO

KLF4 inhibits early neural differentiation of ESCs by coordinating specific 3D chromatin structure, a new mechanism of early neural differentiation

Project description:Circular RNA has been reported to be dynamically expressed during embryonic development and regulates human embryonic stem cells (hESCs), but the identification and regulation of functional circular RNA in mouse embryonic stem cells (mESC) remains unclear. Neural differentiation of embryonic stem cells (ESCs) requires precisely orchestrated gene regulation, a process governed in part by changes in 3D chromatin structure. How these changes regulate gene expression in this context remains unclear. In this study, we observed enrichment of the transcription factor KLF4 at some poised or closed enhancers at TSS-linked regions of genes associated with neural differentiation. Combination analysis of ChIP, HiChIP and RNA-seq data indicated that KLF4 loss in ESCs induced changes in 3D chromatin structure, including increased chromatin interaction loops between neural differentiation-associated genes and active enhancers, leading to upregulated expression of neural differentiation-associated genes and therefore early neural differentiation. This study suggests KLF4 inhibits early neural differentiation by regulation of 3D chromatin structure, which is a new mechanism of early neural differentiation. Conclusions: Our study suggests KLF4 inhibits early neural differentiation by regulation of 3D chromatin structure, which is a new mechanism of early neural differentiation.

2022-09-20 | GSE213418 | GEO

KLF4 inhibits early neural differentiation of ESCs by coordinating specific 3D chromatin structure, a new mechanism of early neural differentiation

Project description:KLF4 inhibits early neural differentiation of ESCs by coordinating specific 3D chromatin structure, a new mechanism of early neural differentiation

| PRJNA880652 | ENA

KLF4 inhibits early neural differentiation of ESCs by coordinating specific 3D chromatin structure.

Project description:Neural differentiation of embryonic stem cells (ESCs) requires precisely orchestrated gene regulation, a process governed in part by changes in 3D chromatin structure. How these changes regulate gene expression in this context remains unclear. In this study, we observed enrichment of the transcription factor KLF4 at some poised or closed enhancers at TSS-linked regions of genes associated with neural differentiation. Combination analysis of ChIP, HiChIP and RNA-seq data indicated that KLF4 loss in ESCs induced changes in 3D chromatin structure, including increased chromatin interaction loops between neural differentiation-associated genes and active enhancers, leading to upregulated expression of neural differentiation-associated genes and therefore early neural differentiation. This study suggests KLF4 inhibits early neural differentiation by regulation of 3D chromatin structure, which is a new mechanism of early neural differentiation.

| S-EPMC9757050 | biostudies-literature

Genome-wide mapping of Klf4 and Klf5 in pluripotent mouse embryonic stem cells (ESCs)

Project description:We identified the binding profile of Klf4 and Klf5, which are both transcription facyors involved in the maintenance of pluripotency of ESCs by inhibiting their differentiation either into endoderm or mesoderm respectively. Undifferentiated mouse ESCs were used to identify Klf4 and Klf5 bidning sites

2014-04-25 | E-GEOD-49848 | biostudies-arrayexpress

Genome-wide mapping of Klf4 and Klf5 in pluripotent mouse embryonic stem cells (ESCs)

2014-04-25 | GSE49848 | GEO

Two enhancers synergistically regulate HoxB genes expressions and retinoic acid-induced early ESCs differentiation through 3D chromatin structure

Project description:Homeobox B cluster (HoxB) genes play important roles in RA-induced early ESCs differentiation. In this study, we identified two enhancers synergistically regulate HoxB genes expressions through 3D chromatin structure and thus regulate RA-induced early ESCs differentiation. 4C data showed interactions between HoxB genes and the two enhancers. CRISPR/Cas9-mediated individual or compound deletion of the two enhancers significantly inhibits HoxB genes expressions while transcriptome analysis revealed that RA induced early ESCs differentiation was blocked in the enhancer KO cells. Our study suggests new mechanism by which two enhancers regulate HoxB genes expressions and retinoic acid-induced early ESCs differentiation through 3D chromatin structure.

2021-03-01 | GSE165725 | GEO

KLF4 binding is involved in the organization and regulation of 3D enhancer networks during acquisition and maintenance of pluripotency.

Project description:Cell fate transitions are accompanied by global transcriptional, epigenetic and topological changes driven by transcription factors (TFs), as is strikingly exemplified by reprogramming somatic cells to pluripotent stem cells (PSCs) via expression of OCT4, KLF4, SOX2 and cMYC. How TFs orchestrate the complex molecular changes around their target gene loci in a temporal manner remains incompletely understood. Here, using KLF4 as a paradigm, we provide the first TF-centric view of chromatin reorganization and its association to 3D enhancer rewiring and transcriptional changes of linked genes during reprogramming of mouse embryonic fibroblasts (MEFs) to PSCs. Inducible depletion of KLF factors in PSCs caused a genome-wide decrease in the connectivity of enhancers, while disruption of individual KLF4 binding sites from PSC-specific enhancers was sufficient to impair enhancer-promoter contacts and reduce expression of associated genes. Our study provides an integrative view of the complex activities of a lineage-specifying TF during a controlled cell fate transition and offers novel insights into the order and nature of molecular events that follow TF binding.

2019-09-03 | PXD014631 | Pride

A Dynamic Interplay of Klf4 Enhancer Elements Drives Naïve-pluripotency

Project description:We characterized a long-range enhancer cluster driving Klf4 expression in naïve pluripotent stem cells. CRISPR/Cas9 mediated screening and genome editing identified DNA motifs corresponding to key pluripotency TFs on these enhancer regions. We employed ChIP-exo genome-wide sequencing to Esrrb and Stat3 in mESCs and validated their functional engagement on the Klf4 enhancer cluster. Moreover, we performed ATAC-seq on wild type and Oct4/Sox2 composite motif biallelic deletion ESCs on Klf4 enhancer E2 to examine the accessible chromatin structure upon loss of lead TFs Oct4 and Sox2 in a single enhancer region.

2018-06-14 | GSE97304 | GEO

Klf4

Project description:Klf4 is the zinc finger transcription factor indispensable for terminal maturation of epithelial tissues and part of group of proteins for the generation of pluripotent embryonic stem cells from differentiated tissues. No definitive in-vivo-function of Klf4 in the hematopoietic system has been established yet. We show here that Klf4 directly guides the transcriptional program for terminal differentiation of Ly-6Chigh monocytes. Klf4 suppresses transcripts of the interferon immune response and induces a proinflammatory cytokine transcriptional program. Concordantly, Klf4 hematopoietic deficiency in mice results in an enhanced Th1 but impaired Th17 immune response, and, consequently, those mice are resistant towards the induction of experimental autoimmune encephalitis (EAE). We here identify Klf4 is a transcription factor required for ontogenesis and function of Ly-6Chigh monocytes at the interface of innate and acquired immunity.

2012-07-31 | GSE11572 | GEO

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