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TET1 and 5-hydroxymethylation preserve the stem cell state of mouse trophoblast

ABSTRACT: TET1 and 5-hydroxymethylation preserve the stem cell state of mouse trophoblast

PROVIDER: PRJNA578148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10302500_1.fastq.gz	Fastqsanger.gz
	SRR10302500_2.fastq.gz	Fastqsanger.gz
	SRR10302501_1.fastq.gz	Fastqsanger.gz
	SRR10302501_2.fastq.gz	Fastqsanger.gz
	SRR10302502_1.fastq.gz	Fastqsanger.gz

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TET1 and 5-Hydroxymethylation Preserve the Stem Cell State of Mouse Trophoblast.

Project description:The ten-eleven translocation factor TET1 and its conferred epigenetic modification 5-hydroxymethylcytosine (5hmC) have important roles in maintaining the pluripotent state of embryonic stem cells (ESCs). We previously showed that TET1 is also essential to maintain the stem cell state of trophoblast stem cells (TSCs). Here, we establish an integrated panel of absolute 5hmC levels, genome-wide DNA methylation and hydroxymethylation patterns, transcriptomes, and TET1 chromatin occupancy in TSCs and differentiated trophoblast cells. We show that the combined presence of 5-methylcytosine (5mC) and 5hmC correlates with transcriptional activity of associated genes. Hypoxia can slow down the global loss of 5hmC that occurs upon differentiation of TSCs. Notably, unlike in ESCs and epiblast cells, most TET1-bound regions overlap with active chromatin marks and TFAP2C binding sites and demarcate putative trophoblast enhancer regions. These chromatin modification and occupancy patterns are highly informative to identify novel candidate regulators of the TSC state.

| S-EPMC7724466 | biostudies-literature

TET1 and 5-hydroxymethylation preserve the stem cell state of mouse trophoblast

Project description:Analysis of 5mC and 5hmC and associated transcription in trophoblast stem cells cultured and differentiated at 20% and 5% oxygen, integrated with previously published datasets

2020-04-23 | GSE139049 | GEO

TET1 modulates trophoblast function by regulation of ODC1 in preeclampsia

Project description:Analysis of trophoblast cell line HTR8/SVneo knocking down the DNA hydroxymethylase TET1. The results provide insights into genes that undergo expression changes in trophoblast cells due to DNA hydroxymethylation.

2025-07-03 | GSE301609 | GEO

TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer [ChIP-seq]

Project description:Ferroptosis, a non-apoptotic programmed cell death marked by iron-dependent lipid peroxidation, is closely associated with cancer. Despite of intensive investigation about the molecular pathways underlying ferroptosis, the mechanism that determines the disparity of cancer cell vulnerability to ferroptosis remains unclear. Here we show that the expression level of TET1, the founding member of the ten-eleven translocation (TET) family of enzymes that mediate DNA 5-hydroxymethylation, determines the susceptibility of cancer cells to ferroptosis. In ferroptosis resistant cells, the expression level of TET1 was remarkably higher than that of the sensitive cells. Cell response to ferroptosis could be affected by interfering TET1 expression. TET1 promoted DNA 5hmC modification at its target gene GCLM, activated both the canonical glutathione (GSH) synthesis, and the non-cannonical γ-glutamyl-peptide accumulation, and thus, protected cancer cells against ferroptosis. Our results uncover the role of TET1 as a ferroptotic defensor in cancer, and suggest the translational potential of targeting the TET/GCLM axis in cancer therapy.

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TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer [5hmC-seq]

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TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer [RNA-seq]

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TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer

Project description:TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer

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A novel role of Tet1/2 proteins in cell cycle progression of trophoblast stem cells

Project description:The ten-eleven translocation (Tet) proteins are well known for their role in maintaining naive pluripotency of embryonic stem cells. Here, we demonstrate that jointly, Tet1 and Tet2 also safeguard the self-renewal potential of trophoblast stem cells (TSCs) and have partially redundant roles in maintaining their epithelial integrity. For the more abundantly expressed Tet1, we demonstrate that this is achieved by binding to critical epithelial genes, notably E-Cadherin, which becomes hyper-methylated and down-regulated in the absence of Tet1. This epithelial-to-mesenchymal transition phenotype is accompanied by centrosome duplication and separation defects. Moreover, we identify a novel role of Tet1 in stabilizing Cyclin B1, thereby acting as a facilitator of mitotic cell cycle progression. As a result, Tet1/2 mutant TSCs are prone to undergo endoreduplicative cell cycles leading to the formation of polyploid trophoblast giant cells. Taken together, our data reveal essential functions of Tet proteins in the trophoblast lineage.

2018-05-02 | GSE109545 | GEO

TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer [ChIP-seq]

Project description:TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer [ChIP-seq]

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TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer [5hmC-seq]

Project description:TET1-mediated DNA hydroxymethylation controlling ferroptosis resistance in cancer [5hmC-seq]

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