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Chip-seq data of mouse Spermatogonia cells of Tet1-ko and WT

ABSTRACT: Chip-seq data of mouse Spermatogonia cells of Tet1-ko and WT

PROVIDER: PRJNA591633 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10530200_1.fastq.gz	Fastqsanger.gz
	SRR10530200_2.fastq.gz	Fastqsanger.gz
	SRR10530201_1.fastq.gz	Fastqsanger.gz
	SRR10530201_2.fastq.gz	Fastqsanger.gz
	SRR10530198_1.fastq.gz	Fastqsanger.gz

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Chip-seq data of mouse Spermatogonia cells of Tet1-ko and WT

Project description:We analysed 2 samples of mouse spermatogonia cells including 3-month-old WT and 3 month-old Tet1

2020-01-18 | GSE140999 | GEO

RNA-seq data of Spermatogonia cells of Tet1-ko and WT

Project description:We analyzed 3 repeats of 12 samples of mouse spermatogonia cells including 3-month-old WT and 3 month-old Tet1, 11-month-old WT and 11-month-old Tet1, aimed to find Tet1 function on male fertility.

2020-01-18 | GSE140014 | GEO

RNA-seq data of Spermatogonia cells of Tet1-ko and WT

Project description:RNA-seq data of Spermatogonia cells of Tet1-ko and WT

| PRJNA588041 | ENA

RNA Sequencing of H1 WT hESCs, H1 QSER1 KO hESCs, H1 TET1 KO hESCs, H1 QSER1/TET1 DKO hESCs, WT Day10 EBs, QSER1 KO Day10 EBs, TET1 KO Day10 EBs, QSER1/TET1 DKO Day10 EBs, WT PP1, QSER1 KO PP1, TET1 KO PP1, and QSER1/TET1 DKO PP1.

Project description:RNA Sequencing of H1 WT hESCs, H1 QSER1 KO hESCs, H1 TET1 KO hESCs, H1 QSER1/TET1 DKO hESCs, WT Day10 embryoid bodies (EBs), QSER1 KO Day10 EBs, TET1 KO Day10 EBs, QSER1/TET1 DKO Day10 EBs, WT pancreatic progenitors (PP1), QSER1 KO PP1, TET1 KO PP1, and QSER1/TET1 DKO PP1. DNA methylation is essential to mammalian development, and dysregulation can cause serious pathological conditions. Key enzymes responsible for deposition and removal of DNA methylation are known, but how they cooperate to tightly regulate the methylation landscape remains a central question. Utilizing a knockin DNA methylation reporter, we performed a genome-wide CRISPR/Cas screen in human embryonic stem cells to discover DNA methylation regulators. The top screen hit was an uncharacterized gene QSER1, which proved to be a key guardian of bivalent promoters and poised enhancers of developmental genes, especially those residing in DNA methylation valleys (or canyons). We further demonstrate cooperation of QSER1 and TET1 through genetic and biochemical interactions to inhibit DNMT3-mediated de novo methylation and safeguard developmental programs.

2021-03-19 | GSE169209 | GEO

Project description:RNA Sequencing of H1 WT hESCs, H1 QSER1 KO hESCs, H1 TET1 KO hESCs, H1 QSER1/TET1 DKO hESCs, WT Day10 EBs, QSER1 KO Day10 EBs, TET1 KO Day10 EBs, QSER1/TET1 DKO Day10 EBs, WT PP1, QSER1 KO PP1, TET1 KO PP1, and QSER1/TET1 DKO PP1.

| PRJNA715661 | ENA

TET1-JMJD3-H3K27me3 targets and regulates Pramel3 to affect spermatogonia self-renewal and proliferation and differentiation

Project description:Histone modification and DNA methylation among epigenetic modifications play a coordinated role in the regulation of spermatogonia. Tet methylcytosine dioxygenase 1 (TET1) can either act as a DNA demethylase, converting 5-methylcytosine to 5-hydroxymethylcytosine or regulate gene expression by forming a complex with other proteins. Increased levels of H3K27me3 will result in transcriptional repression and reduced or silenced protein expression. However, the mechanism by which TET1 mediates the regulation of H3K27me3 in spermatogonia and the target genes that act is not clear. The results of this study showed that the expression of self-renewal-related gene GFRA1 and proliferation-related gene PCNA were up-regulated after JMJD3 overexpression. Moreover, it was demonstrated that TET1 and JMJD3 can interact with H3K27me3 by forming a protein complex, and the CHIP-Seq sequencing results analyzed that TET1 targets and regulates the Pramel3 gene when interacting with H3K27me3, and TET1 overexpression promotes the up-regulation of Pramel3 expression. Our study identified a novel link between TET1 and H3K27me3 and established a TET1-JMJD3-H3K27me3-Pramel3 regulatory axis to regulate spermatogonia self-renewal, proliferation and differentiation. It provides a new idea to further investigate the mechanism of spermatogenesis and spermatogenic disorders from the epigenetic level.

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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.

2022-08-31 | PXD028850 | Pride

Dissection of TET1 catalytic and non-catalytic functions reveals DNA demethylation independent gene and ERV regulation

Project description:Surveillance 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 understanding of DNA methylation dynamics. Interestingly, in recent years evidence accumulated that TET1 also harbours non-catalytic functions. However, the role and mechanism of TET1 DNA demethylation independent functions still remain poorly understood. Here, we use genome engineering and quantitative multi-omics approaches to dissect the non-catalytic role of TET1. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. To gain insights into possible mechanisms by which TET1 regulates transcription independent of DNA demethylation, we asked if the loss of TET1 is accompanied by changes in the histone modificaiton landscape. To this end, we compared the relative abundances of core histone modifications between Tet1 KO, Tet1 CM and WT mESCs using quantitative LC-MS/MS analysis. Surprisingly, we observed a profound global reduction of pH4Kac and H4K20me3 as well as H3K27me3 in Tet1 KO mESC. Vice versa, the monomethylation states of the latter two residues, H3K27me1 and H4K20me1 were significantly increased in Tet1 KO. Similar to the results from the transcriptome data, most of these changes were specific to Tet1 KO cells.

2022-08-11 | PXD028566 | Pride

TET1 KO affects Sox9 function

Project description:TET1 KO affects Sox9 function

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Tet1 regulates embryonic stem cell differentiation programs and development independent of its catalytic activity.

Project description:In this study: (1) we characterized the Tet1 non-catalytic functions in the regulation of ESC gene expression programs by performing transcriptomic analysis of Tet1 wild type (WT), Tet1 catalytic mutant (Mut) and Tet1 knockout (KO) mouse ESCs by RNA-seq to identify differentially expressed genes. (2) We mapped the genome-wide occupancy of endogenously FLAG-tagged Tet1-WT and Tet1-Mut in ESCs by CUT&Tag using a specific antibody against FLAG. (3) We determined how the genome-wide occupancy of the epigenetic modifiers: Ezh2, Sin3a, Chd4 and the enrichment of histone marks: H3K27me3, H3K4me3 and H3K27ac, are affected in Tet1-KO ESCs versus Tet1-WT and Tet1-Mut by CUT&Tag or CUT&RUN. (4) We analyzed methylation levels and distribution in Tet1-WT, Tet1-Mut and Tet1-KO ESCs by WGBS, to confirm Tet1 non-catalytic targets with no differential methylation. (5) We explored whether Tet1 non-catalytic functions play a role in chromatin accessibility by performing ATAC-seq in Tet1-WT, Tet1-Mut and Tet1-KO ESCs.

2022-01-25 | GSE176389 | GEO

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