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ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [RNA-Seq]

ABSTRACT: ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [RNA-Seq]

PROVIDER: PRJNA648061 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12303072_1.fastq.gz	Fastqsanger.gz
	SRR12303072_2.fastq.gz	Fastqsanger.gz
	SRR12303073_1.fastq.gz	Fastqsanger.gz
	SRR12303073_2.fastq.gz	Fastqsanger.gz
	SRR12303074_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [RNA-Seq]

Project description:Metazoan transcription factors typically regulate large numbers of genes. Here we identify via a CRISPR-Cas9 genetic screen ZNF410, a pentadactyl DNA binding protein that in human erythroid cells directly and measurably activates only one gene, the NuRD component CHD4. Specificity is conveyed by two highly evolutionarily conserved clusters of ZNF410 binding sites near the CHD4 gene with no counterparts elsewhere in the genome. Loss of ZNF410 in adult type human erythroid cell culture systems and xenotransplant settings diminishes CHD4 levels and derepresses the fetal hemoglobin genes. While previously known to be silenced by CHD4, the fetal globin genes are exposed here as among the most sensitive to reduced CHD4 levels. In vitro DNA binding assays and crystallographic studies reveal the ZNF410-DNA binding mode. ZNF410 is a remarkably selective transcriptional activator in erythroid cells whose perturbation might offer new therapeutic opportunities in the treatment of hemoglobinopathies.

2020-12-09 | GSE154961 | GEO

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [ChIP-Seq]

2020-12-09 | GSE154960 | GEO

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression

Project description:ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression

| PRJNA648059 | ENA

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [ChIP-Seq]

Project description:ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [ChIP-Seq]

| PRJNA648058 | ENA

ZNF410 Uniquely Activates the NuRD Component CHD4 to Silence Fetal Hemoglobin Expression.

Project description:Metazoan transcription factors typically regulate large numbers of genes. Here we identify via a CRISPR-Cas9 genetic screen ZNF410, a pentadactyl DNA-binding protein that in human erythroid cells directly activates only a single gene, the NuRD component CHD4. Specificity is conveyed by two highly evolutionarily conserved clusters of ZNF410 binding sites near the CHD4 gene with no counterparts elsewhere in the genome. Loss of ZNF410 in adult-type human erythroid cell culture systems and xenotransplantation settings diminishes CHD4 levels and derepresses the fetal hemoglobin genes. While previously known to be silenced by CHD4, the fetal globin genes are exposed here as among the most sensitive to reduced CHD4 levels.. In vitro DNA binding assays and crystallographic studies reveal the ZNF410-DNA binding mode. ZNF410 is a remarkably selective transcriptional activator in erythroid cells, and its perturbation might offer new opportunities for treatment of hemoglobinopathies.

| S-EPMC8556680 | biostudies-literature

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression

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

2020-12-09 | GSE154963 | GEO

Gene expression profiling of HUDEP-2 cells edited with either ZNF410 targeting or control sgRNA

Project description:RNA sequencing was performed of HUDEP-2 cells edited at either ZNF410 or AAVS1 (control locus) to measure gene expression changes due to loss of ZNF410 expression. CHD4 was the most significantly downregulated gene upon ZNF410 editing. We observed that ZNF410 binds to DNA upstream of the CHD4 gene. To test the requirement of ZNF410 binding for CHD4 expression we generated a HUDEP-2 clone in which this region of ZNF410 binding was deleted (CHD4 6.7 kb element deletion clone). We performed RNA-seq of CHD4 6.7 kb element deleted HUDEP-2 cells after either ZNF410 or AAVS1 (control locus) editing and only observed 2 differentially expressed genes after ZNF410 editing in CHD4 6.7 kb element deletion cells, consistent with our results that nearly all gene expression changes found after ZNF410 editing are due to changes in CHD4 expression.

2021-02-05 | GSE166222 | GEO

ZFHX4 and CHD4 ChIP sequencing in glioblastoma tumor initiating cells

Project description:Glioblastomas (GBM) harbor subpopulations of therapy-resistant tumor initiating cells (TICs) that are self-renewing and multipotent. To understand the regulation of the TIC state, we performed an image-based screen for genes regulating GBM TIC maintenance and identified ZFHX4, a 397-kDa transcription factor. ZFHX4 is required to maintain TIC-associated phenotypes in vitro, suggesting that ZFHX4 regulates TIC differentiation, and its suppression increases glioma-free survival in intracranial xenografts. ZFHX4 interacts with CHD4, a core member of the NuRD (nucleosome remodeling and deacetylase) complex. ZFHX4 and CHD4 bind to overlapping sets of genomic loci and control similar gene expression programs. Using expression data derived from GBM patients, we demonstrate ZFHX4 is a master regulator of CHD4-mediated gene expression. These observations define ZFHX4 as a regulatory factor that links the chromatin remodeling NuRD complex and the GBM TIC state. Examination of binding of ZFHX4 and CHD4 across the human genome, using the 0308 tumor initiating cell line. Two replicates for each protein, compared to whole cell extract inputs.

2014-01-16 | E-GEOD-52419 | biostudies-arrayexpress

ChIPseq and RNAseq analysis of T47D cells with/without silencing TRPS1/CHD4

Project description:We reported the transcriptional regulation function and mechanism of TRPS1-CHD4/NuRD.

2018-12-26 | GSE114213 | GEO

Identification and characterization of novel proteins associated with CHD4

Project description:CHD (chromodomain helicase DNA binding protein) family is composed of nine members of chromatin remodeling factors that regulate chromatin structure in an ATP-dependent manner. Among them, CHD4 contributes to many basic cellular functions during development mainly through multiple proteins interacting with CHD4 including NuRD (nucleosome remodeling and deacetylase activities) complex, which contains histone deacetylase HDAC1/2. However, functions of CHD4 that are not mediated by NuRD complexes have also been found, implying the existence of unknown proteins that are associated with CHD4. In the present study, we generated CHD4 FLAG-tag knock-in cells in HeLa-S3 and HEK293T cells and sought proteins bound to CHD4 with the use of immunoprecipitation and liquid chromatography and tandem MS (LC-MS/MS) analysis. We found that LCORL (ligand dependent nuclear receptor corepressor like) and NOL4L (nucleolar protein 4 like) were reproducibly identified as a novel CHD4 interactors. RNA-sequencing analysis of HEK293T cells depleted of CHD4, LCORL, and NOL4L revealed consistent upregulation of genes related to the Notch pathway. Our results thus suggest that both NOL4L and LCORL may cooperate with CHD4 to suppress the Notch pathway in mammalian cells.

2022-01-01 | GSE190369 | GEO

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