CHD7 binds to insulators during neuronal differentiation [RNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1244029 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32915109_1.fastq.gz | Fastqsanger.gz | |||
| SRR32915109_2.fastq.gz | Fastqsanger.gz | |||
| SRR32915110_1.fastq.gz | Fastqsanger.gz | |||
| SRR32915110_2.fastq.gz | Fastqsanger.gz | |||
| SRR32915111_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:CHD7 binds to insulators during neuronal differentiation [CUT&Tag]
| PRJNA1244028 | ENA
Project description:Spiral ganglion neurons (SGNs) are crucial for hearing, and the loss of SGNs causes hearing loss. Stem cell-based therapies offer a promising approach for SGN regeneration and require understanding the mechanisms governing SGN differentiation. We investigated the chromatin remodeler CHD7 in SGN differentiation using immortalized multipotent otic progenitor (iMOP) cells. We demonstrate that CHD7 knockdown significantly impairs neuronal differentiation. Genome-wide analysis reveals CHD7 enrichment at diverse cis-regulatory elements, with notable enrichment at sites marked by the insulator-binding protein CTCF between topologically associating domains (TADs). Insulators marked by the enrichment of CHD7 and CTCF resided near genes critical for neuronal differentiation, including Mir9-2. Targeting these regulatory regions in iMOPs with CRISPR interference (CRISPRi) and activation (CRISPRa) increased miR9 transcription, irrespective of the method. The occlusion of the regulatory elements suggested that the insulators function to regulate gene expression. The study highlights CHD7 activity at insulators and underscores its importance in promoting neuronal differentiation.
2025-04-07 | GSE293324 | GEO
Project description:Spiral ganglion neurons (SGNs) are crucial for hearing, and the loss of SGNs causes hearing loss. Stem cell-based therapies offer a promising approach for SGN regeneration and require understanding the mechanisms governing SGN differentiation. We investigated the chromatin remodeler CHD7 in SGN differentiation using immortalized multipotent otic progenitor (iMOP) cells. We demonstrate that CHD7 knockdown significantly impairs neuronal differentiation. Genome-wide analysis reveals CHD7 enrichment at diverse cis-regulatory elements, with notable enrichment at sites marked by the insulator-binding protein CTCF between topologically associating domains (TADs). Insulators marked by the enrichment of CHD7 and CTCF resided near genes critical for neuronal differentiation, including Mir9-2. Targeting these regulatory regions in iMOPs with CRISPR interference (CRISPRi) and activation (CRISPRa) increased miR9 transcription, irrespective of the method. The occlusion of the regulatory elements suggested that the insulators function to regulate gene expression. The study highlights CHD7 activity at insulators and underscores its importance in promoting neuronal differentiation.
2025-04-07 | GSE293323 | GEO
Project description:The chromodomain helicase DNA binding protein 7 (CHD7) is a nucleosome repositioner implicated in multiple cellular processes, including neuronal differentiation. We identified CHD7 marked sites at TAD boundaries that regulate neuronal differentiation in an otic stem cell line. We showed that CHD7 co-occupied CTCF sites genome-wide. We identified CTCF+ CHD7+ sites near an essential transcription factor, Sox11, required for otic neuronal differentiation. The Sox11 promoter and 3’ untranslated region (UTR) showed CHD7 enrichment. The CHD7-marked sites at the 3’UTR displayed histone marks corresponding to active transcription that resulted in Sox11 antisense transcripts. Blocking the singular CHD7-marked site with CRISPRi decreased neurite lengths, reduced neuronal marker expression (TUBB3), and attenuated Sox11 antisense transcripts. Sox11 antisense transcripts were previously suggested to form double-stranded RNA and degrade the Sox11 transcript. Surprisingly, the level of the Sox11 sense transcripts remained unaffected after CRISPRi. We propose that CHD7 at TAD boundaries modulate the chromatin accessibility of CTCF-marked insulators, altering the 3D chromatin organization and ultimately affecting gene expression. Our results implicate a general mechanism of CHD7 in facilitating neuronal differentiation and provide insight into CHD7 dysfunction in CHARGE syndrome, an intellectual developmental disability disorder.
2025-04-07 | GSE293439 | GEO
Project description:The chromodomain helicase DNA binding protein 7 (CHD7) is a nucleosome repositioner implicated in multiple cellular processes, including neuronal differentiation. We identified CHD7 marked sites at TAD boundaries that regulate neuronal differentiation in an otic stem cell line. We showed that CHD7 co-occupied CTCF sites genome-wide. We identified CTCF+ CHD7+ sites near an essential transcription factor, Sox11, required for otic neuronal differentiation. The Sox11 promoter and 3’ untranslated region (UTR) showed CHD7 enrichment. The CHD7-marked sites at the 3’UTR displayed histone marks corresponding to active transcription that resulted in Sox11 antisense transcripts. Blocking the singular CHD7-marked site with CRISPRi decreased neurite lengths, reduced neuronal marker expression (TUBB3), and attenuated Sox11 antisense transcripts. Sox11 antisense transcripts were previously suggested to form double-stranded RNA and degrade the Sox11 transcript. Surprisingly, the level of the Sox11 sense transcripts remained unaffected after CRISPRi. We propose that CHD7 at TAD boundaries modulate the chromatin accessibility of CTCF-marked insulators, altering the 3D chromatin organization and ultimately affecting gene expression. Our results implicate a general mechanism of CHD7 in facilitating neuronal differentiation and provide insight into CHD7 dysfunction in CHARGE syndrome, an intellectual developmental disability disorder.
2025-04-07 | GSE293438 | GEO
Project description:The chromodomain helicase DNA binding protein 7 (CHD7) is a nucleosome repositioner implicated in multiple cellular processes, including neuronal differentiation. We identified CHD7 marked sites at TAD boundaries that regulate neuronal differentiation in an otic stem cell line. We showed that CHD7 co-occupied CTCF sites genome-wide. We identified CTCF+ CHD7+ sites near an essential transcription factor, Sox11, required for otic neuronal differentiation. The Sox11 promoter and 3’ untranslated region (UTR) showed CHD7 enrichment. The CHD7-marked sites at the 3’UTR displayed histone marks corresponding to active transcription that resulted in Sox11 antisense transcripts. Blocking the singular CHD7-marked site with CRISPRi decreased neurite lengths, reduced neuronal marker expression (TUBB3), and attenuated Sox11 antisense transcripts. Sox11 antisense transcripts were previously suggested to form double-stranded RNA and degrade the Sox11 transcript. Surprisingly, the level of the Sox11 sense transcripts remained unaffected after CRISPRi. We propose that CHD7 at TAD boundaries modulate the chromatin accessibility of CTCF-marked insulators, altering the 3D chromatin organization and ultimately affecting gene expression. Our results implicate a general mechanism of CHD7 in facilitating neuronal differentiation and provide insight into CHD7 dysfunction in CHARGE syndrome, an intellectual developmental disability disorder.
2025-04-07 | GSE293437 | GEO
Project description:CHD7 marks TAD boundaries during neuronal differentiation [RNA-Seq]
| PRJNA1244620 | ENA
Project description:CHD7 marks TAD boundaries during neuronal differentiation [ChIP-Seq]
| PRJNA1244622 | ENA
Project description:CHD7 marks TAD boundaries during neuronal differentiation [Cut & Tag]
| PRJNA1244626 | ENA
Project description:Chromodomain helicase DNA-binding protein 7 (CHD7) is an ATP-dependent chromatin remodeling enzyme, functioning as chromatin reader to conduct epigenetic modification. Its effect on osteogenic differentiation of human dental follicle cells (hDFCs) remains unclear. Here we show CHD7 expression increases with osteogenic differentiation. knockdown of CHD7 impairs the osteogenic ability of hDFCs, characterized by reduced alkaline phosphatase activity and mineralization, and decreased expression of osteogenesis-related genes. Conversely, CHD7 overexpression enhances the osteogenic differentiation of hDFCs. Mechanically, RNA-seq analyses revealed the down-regulated enrichment of PTH (parathyroid hormone)/PTH1R (parathyroid hormone receptor-1) signaling pathway after CHD7 knockdown. We found the expression of PTH1R positively correlates with CHD7. Importantly, overexpression of PTH1R in CHD7-knockdown hDFCs partially rescued the impaired osteogenic differentiation. Our research demonstrates that CHD7 regulates the osteogenic differentiation of hDFCs by regulating the transcription of PTH1R.
2020-07-22 | GSE154822 | GEO