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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

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 [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 [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

SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity [ATAC-Seq]

Project description:Clustering of multiple transcription factor binding sites (TFBSs) for the same TF has proved to be a pervasive feature of cis-regulatory elements in eukaryotic genome. However, contribution of binding sites within the homotypic clusters of TFBSs (HCTs) to TF binding and target gene expression remains to be understood. Here, we characterize the CHD4 enhancers that harbor unique functional ZNF410 HCTs genome-wide. We uncover that ZNF410 controls chromatin accessibility and activity of the CHD4 enhancer regions. We demonstrate that ZNF410 binds to the HCTs in a collaborative fashion, further conferring transcriptional activation. Especially, three ZNF410 motifs (sub-HCTs) located at 3´ end of the distal enhancer act as “switch motifs” to control the chromatin accessibility and enhancer activity. Mechanistically, SWI/SNF complex is selectively required to mediate cooperative ZNF410 binding for CHD4 expression. Together, our findings expose a complex functional hierarchy of homotypic clustered motifs, which cooperates to fine-tune target gene expression.

2025-03-22 | GSE256317 | GEO

SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity [RNA-Seq]

2025-03-22 | GSE256315 | GEO

SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity [ChIP-Seq]

2025-03-22 | GSE256316 | GEO