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Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

ABSTRACT: Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

PROVIDER: PRJNA788624 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17223935.fastq.gz	Fastqsanger.gz
	SRR17223937.fastq.gz	Fastqsanger.gz
	SRR17223939.fastq.gz	Fastqsanger.gz
	SRR17223940.fastq.gz	Fastqsanger.gz
	SRR17223942.fastq.gz	Fastqsanger.gz

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Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

Project description:Here we report both TET1-WT and catalytically dead mutant TET1 (TET1-MUT) directly interact with STAT5B in PDX2 B-ALL cells. To study the landscape of TET1 and STAT5B binding in whole genomic DNA and test if the STAT5B binding signal is affected by TET1, we conduct the ChIP-seq assay with flag antibody (TET1-WT, TET1-MUT) and STAT5B antibody (sgNS or sgTET1) respectively. The results showed that TET1 bound peaks overlap with STAT5B very well and the tag density of STAT5B on target genes decreases in TET1-impeded cells. We conclude that TET1 recruit STAT5B to the promoters of its target genes and further promote the target genes’ transcriptions.

2023-02-13 | GSE190852 | GEO

Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

Project description:Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

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Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells; Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

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

2023-02-13 | GSE190853 | GEO

Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells

Project description:Here we report that TET1 has a critical role in B-ALL development. TET1-depleted cells delayed the onset of B-ALL. To investigate the mechanisms, we first generate the patient-derived xenograft cells (PDX2) and transduce with inducible-Cas9 and sgRNA targeting TET1. After treatment with doxycycline, we observe the expression of Cas9 and a depletion of TET1 protein. By using the high throughput sequencing RNA-seq, we check the potential targets of TET1 in B-ALL cells. Finally, we validate that CD72 and JCHAIN are two essential targets of TET1 signaling in B-ALL cells.

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Genetic STAT5B immunodysregulatory disorder

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TET1 interactome in mESCs (via ChIP-MS)

Project description:Precise regulation of DNA methylation in mammals is critical for genome stability and epigenetic regulation. The discovery of the ten-eleven translocation (TET) proteins catalyzing the oxidation from 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) revolutionized the perspective on the complexity and regulation of DNA modifications. Despite accumulating knowledge about the role of TET1, it remains unclear to what extent these can be attributed to its catalytic activity. Here, we use genome engineering and quantitative multi-omics approaches to dissect the role and mechanism of TET1 in mESCs. Our study identifies TET1 as an essential interaction hub for multiple chromatin modifying complexes and as a global regulator of histone modifications. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. Moreover, we show that the establishment of H3K9me3 and H4K20me3 at ERV1, ERVK, and ERVL is mediated by TET1 independent of DNA demethylation. We provide evidence that repression of endogenous retroviruses depends on the interaction between TET1 and SIN3A. In summary, we demonstrate that the non-catalytic functions of TET1 are critical for regulation of gene expression and the silencing of endogenous retroviruses in mESCs.

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