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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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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

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

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

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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.

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

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

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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.

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OGT, H2B S112GlcNAc, TET2 ChIP-seq results

Project description:TET2 directly interacts with OGT, which is important for the chromatin association of OGT in vivo. Although this specific interaction does not regulate the enzymatic activity of TET2, it facilitates OGT-dependent histone O-GlcNAcylation. Moreover, OGT associates with TET2 at transcription starting sites (TSS). Down-regulation of TET2 reduces the amount of H2B S112 GlcNAc marks in vivo, which are associated with gene transcription regulation. We found that OGT interacts with TET2 tightly. Using ChIP-seq with specific antibodies, we tested the co-localization of TET2 and OGT in genome level.

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