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Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells

ABSTRACT: Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells

PROVIDER: PRJNA489876 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7807380.fastq.gz	Fastqsanger.gz
	SRR7807381.fastq.gz	Fastqsanger.gz
	SRR7807382.fastq.gz	Fastqsanger.gz
	SRR7807384.fastq.gz	Fastqsanger.gz
	SRR7807384_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells (WGBS)

Project description:Whole genome bisulfite sequencing of wild type embryonic stem cells and cells bearing a mutation that perturbs the OGT-TET1 interaction

2018-10-29 | GSE119665 | GEO

Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells (RNA-Seq)

Project description:RNA-seq of wild type embryonic stem cells and cells bearing a mutation that perturbs the OGT-TET1 interaction

2018-10-29 | GSE109540 | GEO

Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells (WGBS)

Project description:Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells (WGBS)

| PRJNA489878 | ENA

Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells (RNA-Seq)

Project description:Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells (RNA-Seq)

| PRJNA431358 | ENA

OGT binds a conserved C-terminal domain of TET1 to regulate TET1 activity and function in development

Project description:TET enzymes convert 5-methylcytosine to 5-hydroxymethylcytosine and higher oxidized derivatives. TETs stably associate with and are post-translationally modified by the nutrient-sensing enzyme OGT, suggesting a connection between metabolism and the epigenome. Here, we show for the first time that modification by OGT enhances TET1 activity in vitro. We identify a a domain of TET1 domain that is responsible necessary and sufficient for binding to OGT and report a point mutation that disrupts the TET1-OGT interaction. We show that the TET1-OGTthis interaction is necessary for TET1 to rescue hematopoetic stem cell production in tet mutant zebrafish embryos, suggesting that OGT promotes TET1’s function during development. Finally, we show that disrupting the TET1-OGT interaction in mouse embryonic stem cells changes the abundance of TET-containing high molecular weight complexesTET2 and 5-methylcytosine, which is accompanied by alterations in gene expression and causes widespread gene expression changes. These results link metabolism and epigenetic control, which may be relevant to the developmental and disease processes regulated by these two enzymes.

2018-11-02 | GSE119500 | GEO

OGT prevents DNA demethylation and suppresses the expression of transposable elements in heterochromatin by restraining TET activity genome-wide

Project description:The O-GlcNAc transferase OGT interacts robustly with all three mammalian TET methylcytosine dioxygenases. We show here that deletion of the Ogt gene in mouse embryonic stem cells (mESC) results in a widespread increase in the TET product 5-hydroxymethylcytosine (5hmC) in both euchromatic and heterochromatic compartments, with concomitant reduction of the TET substrate 5-methylcytosine (5mC) at the same genomic regions. mESC treated with an OGT inhibitor displayed increased 5hmC, and attenuating the TET1-OGT interaction in mESC resulted in a genome-wide decrease of 5mC, indicating that OGT restrains TET activity and limits untoward DNA demethylation in a manner that requires the TET-OGT interaction and the catalytic activity of OGT. DNA hypomethylation in OGT-deficient cells was accompanied by de-repression of transposable elements (TEs) predominantly located in heterochromatin. We suggest that OGT protects the genome against TET-mediated DNA demethylation and loss of heterochromatin integrity, preventing the aberrant increase in TE expression noted in cancer, autoimmune-inflammatory diseases, cellular senescence and ageing.

2025-01-26 | GSE247534 | GEO

Perturbation of the OGT-TET1 interaction in mouse embryonic stem cells

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

2018-10-29 | GSE119666 | GEO

OGT prevents DNA demethylation and suppresses the expression of transposable elements in heterochromatin by restraining TET activity genome-wide (WGBS)

Project description:The O-GlcNAc transferase OGT interacts robustly with all three mammalian TET methylcytosine dioxygenases. We show here that deletion of theOgtgene in mouse embryonic stem cells (mESC) results in a widespread increase in the TET product 5-hydroxymethylcytosine (5hmC) in both euchromatic and heterochromatic compartments, with concomitant reduction of the TET substrate 5-methylcytosine (5mC) at the same genomic regions. mESC engineered to abolish the TET1-OGT interaction likewise displayed a genome-wide decrease of 5mC. DNA hypomethylation in OGT-deficient cells was accompanied by de-repression of transposable elements (TEs) predominantly located in heterochromatin, and this increase in TE expression was sometimes accompanied by increased cis-expression of genes and exons located 3’ of the expressed TE. Thus, the TET-OGT interaction prevents DNA demethylation and TE expression in heterochromatin by restraining TET activity genome-wide. We suggest that OGT protects the genome against DNA hypomethylation and impaired heterochromatin integrity, preventing the aberrant increase in TE expression observed in cancer, autoimmune-inflammatory diseases, cellular senescence and ageing.

2025-01-01 | GSE252759 | GEO

OGT prevents DNA demethylation and suppresses the expression of transposable elements in heterochromatin by restraining TET activity genome-wide (RNA-Seq)

Project description:The O-GlcNAc transferase OGT interacts robustly with all three mammalian TET methylcytosine dioxygenases. We show here that deletion of theOgtgene in mouse embryonic stem cells (mESC) results in a widespread increase in the TET product 5-hydroxymethylcytosine (5hmC) in both euchromatic and heterochromatic compartments, with concomitant reduction of the TET substrate 5-methylcytosine (5mC) at the same genomic regions. mESC engineered to abolish the TET1-OGT interaction likewise displayed a genome-wide decrease of 5mC. DNA hypomethylation in OGT-deficient cells was accompanied by de-repression of transposable elements (TEs) predominantly located in heterochromatin, and this increase in TE expression was sometimes accompanied by increased cis-expression of genes and exons located 3’ of the expressed TE. Thus, the TET-OGT interaction prevents DNA demethylation and TE expression in heterochromatin by restraining TET activity genome-wide. We suggest that OGT protects the genome against DNA hypomethylation and impaired heterochromatin integrity, preventing the aberrant increase in TE expression observed in cancer, autoimmune-inflammatory diseases, cellular senescence and ageing.

2025-01-01 | GSE252758 | GEO

OGT prevents DNA demethylation and suppresses the expression of transposable elements in heterochromatin by restraining TET activity genome-wide (CMS-IP)

Project description:The O-GlcNAc transferase OGT interacts robustly with all three mammalian TET methylcytosine dioxygenases. We show here that deletion of theOgtgene in mouse embryonic stem cells (mESC) results in a widespread increase in the TET product 5-hydroxymethylcytosine (5hmC) in both euchromatic and heterochromatic compartments, with concomitant reduction of the TET substrate 5-methylcytosine (5mC) at the same genomic regions. mESC engineered to abolish the TET1-OGT interaction likewise displayed a genome-wide decrease of 5mC. DNA hypomethylation in OGT-deficient cells was accompanied by de-repression of transposable elements (TEs) predominantly located in heterochromatin, and this increase in TE expression was sometimes accompanied by increased cis-expression of genes and exons located 3’ of the expressed TE. Thus, the TET-OGT interaction prevents DNA demethylation and TE expression in heterochromatin by restraining TET activity genome-wide. We suggest that OGT protects the genome against DNA hypomethylation and impaired heterochromatin integrity, preventing the aberrant increase in TE expression observed in cancer, autoimmune-inflammatory diseases, cellular senescence and ageing.

2025-01-01 | GSE252757 | GEO

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