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Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3

ABSTRACT: Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3

PROVIDER: PRJNA789532 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17247774_1.fastq.gz	Fastqsanger.gz
	SRR17247774_2.fastq.gz	Fastqsanger.gz
	SRR17247775_1.fastq.gz	Fastqsanger.gz
	SRR17247775_2.fastq.gz	Fastqsanger.gz
	SRR17247776_1.fastq.gz	Fastqsanger.gz

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Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3 (Whole Genome Sequencing [Low Coverage])

Project description:Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3 (Whole Genome Sequencing [Low Coverage])

| PRJNA885142 | ENA

Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3

Project description:Gene expression with RNA-seq for inducible Tet TKO (Tet iTKO) mESCs compared with control mouse ESCs (mESC) after 6.5 days in vitro culture after tamoxifen treatment

2022-10-28 | GSE191045 | GEO

Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3.

Project description:TET (Ten-Eleven Translocation) dioxygenases effect DNA demethylation through successive oxidation of the methyl group of 5-methylcytosine (5mC) in DNA. In humans and in mouse models, TET loss-of-function has been linked to DNA damage, genome instability and oncogenesis. Here we show that acute deletion of all three Tet genes, after brief exposure of triple-floxed, Cre-ERT2-expressing mouse embryonic stem cells (mESC) to 4-hydroxytamoxifen, results in chromosome mis-segregation and aneuploidy; moreover, embryos lacking all three TET proteins showed striking variation in blastomere numbers and nuclear morphology at the 8-cell stage. Transcriptional profiling revealed that mRNA encoding a KH-domain protein, Khdc3 (Filia), was downregulated in triple TET-deficient mESC, concomitantly with increased methylation of CpG dinucleotides in the vicinity of the Khdc3 gene. Restoring KHDC3 levels in triple Tet-deficient mESC prevented aneuploidy. Thus, TET proteins regulate Khdc3 gene expression, and TET deficiency results in mitotic infidelity and genome instability in mESC at least partly through decreased expression of KHDC3.

| S-EPMC9584922 | biostudies-literature

Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3 (Whole Genome Sequencing [Low Coverage])

Project description:Low coverage whole genome sequencing (lc-WGS) from inducible Tet TKO (Tet iTKO) and control (Ctrl) mouse ESCs (mESC), as well as for germline Dnmt TKO mESCs. mESCs were sorted to isolate the Live/Dead dye and Thy1.2 negative CD326+GFP+ population representing the mESCs populations responsive to the tamoxifen treatment. The cells were resuspended in FACS buffer and filtered with a 70 µM filter before sorting. These bulk-population samples were analyzed by using low coverage Whole Genome Sequencing (lc-WGS).

2022-10-01 | GSE214402 | GEO

Tet enzymes are essential for embryogenesis and completion of embryonic genome activation

Project description:Mammalian embryo development begins in transcriptional silence followed by activation of thousands of genes. Reprogramming of DNA methylation is integral to embryogenesis and linked to Tet enzymes; however, their function in early development is not fully understood. Here, we generated combined deficiencies of all three Tet enzymes in mouse oocytes and observed arrest at 2-cell stage with the most severe phenotype linked to Tet2. Gene expression analysis revealed that Tet enzymes are required for completion of embryonic genome activation. Our results demonstrate that Tet enzymes have non-redundant roles and are key components of EGA in mammalian embryos.

2021-11-22 | GSE57063 | GEO

Loss of Tet enzymes compromises proper differentiation of embryonic stem cells

Project description:Tet enzymes (Tet1/2/3) catalyze the conversion of 5-methylcytosine (5mC) to 5-hydroxy-methylcytosine (5hmC) and are dynamically expressed in various embryonic and adult cell types. While loss of individual Tet enzymes or combined deficiency of Tet1/2 allows for embryogenesis, the effect of complete loss of Tet activity and 5hmC marks in development has not been established. To define the role of Tet enzymes and 5hmC in development we have generated Tet1, Tet2 and Tet3 triple knockout (TKO) mouse embryonic stem cells (ESCs) and examined their developmental potential in vitro and in vivo. Combined deficiency of all three Tet enzymes led to complete depletion of 5hmC and impaired ESC differentiation as seen in poorly differentiated TKO embryoid bodies and teratomas. Consistent with impaired differentiation, TKO ES cells exhibited limited contribution to the chimeric embryos and could not support embryonic development in tetraploid complementation assays. Gene expression profiles and genome wide methylome analyses of TKO embryoid bodies revealed promoter hypermethylation and deregulation of genes implicated in embryonic development and differentiation. These findings suggest a requirement for Tet and 5hmC-mediated DNA demethylation in proper regulation of gene expression during differentiation of embryonic stem cells and development. Methylation patterns in tissue samples from a series of wt and Tet1/Tet2 DKO embryos, neonates and adults were generated using ethylated DNA immunoprecipitation with antibodies against 5mC (MeDIP) and 5hmC (hMeDIP) followed by deep sequencing.

2014-04-17 | E-GEOD-55049 | biostudies-arrayexpress

Loss of Tet enzymes compromises proper differentiation of embryonic stem cells

2014-04-17 | GSE55049 | GEO

Tet enzymes are required for mammalian embryonic hematopoiesis

Project description:In this study we have examined the role of Tet enzymes in regulation of embryonic Endothelial cells (ECs) and Hematopoietic stem and progenitor cells (HSPCs). We have performed transcriptomic and methylation analyses of Tet deficient and wild type ECs and HSPCs isolated from E11.5 embryonic aorta-gonad-mesonephros (AGM) to identify differentially expressed genes and differentially methylated regions.

2022-02-19 | GSE176391 | GEO

Tet enzymes are required for mammalian embryonic hematopoiesis

Project description:Tet enzymes are required for mammalian embryonic hematopoiesis

| PRJNA736061 | ENA

TET enzymes augment AID expression via 5hmC modifications at the Aicda superenhancer [ATAC-seq]

Project description:TET enzymes are dioxygenases that promote DNA demethylation by oxidizing the methyl group of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Here we report a close correspondence between 5hmC-marked regions, chromatin accessibility and enhancer activity in B cells, and a strong enrichment for consensus binding motifs for basic region-leucine zipper (bZIP) transcription factors at TET-responsive genomic regions. Functionally, Tet2 and Tet3 regulate class switch recombination (CSR) in murine B cells by enhancing expression of Aicda, encoding the cytidine deaminase AID essential for CSR. TET enzymes deposit 5hmC, demethylate and maintain chromatin accessibility at two TET-responsive elements, TetE1 and TetE2, located within a superenhancer in the Aicda locus. Transcriptional profiling identified BATF as the bZIP transcription factor involved in TET-dependent Aicda expression. 5hmC is not deposited at TetE1 in activated Batf-deficient B cells, indicating that BATF recruits TET proteins to the Aicda enhancer. Our data emphasize the importance of TET enzymes for bolstering AID expression, and highlight 5hmC as an epigenetic mark that captures enhancer dynamics during cell activation.

2019-04-29 | GSE116203 | GEO

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