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RNA-seq of primary mouse monocytes from miR-150 knockout and Tet3 knockout mice compared to wild type controls

ABSTRACT: RNA-seq of primary mouse monocytes from miR-150 knockout and Tet3 knockout mice compared to wild type controls

PROVIDER: PRJEB29201 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2843720_1.fastq.gz	Fastqsanger.gz
	ERR2843720_2.fastq.gz	Fastqsanger.gz
	ERR2843730_1.fastq.gz	Fastqsanger.gz
	ERR2843730_2.fastq.gz	Fastqsanger.gz
	ERR2843740_1.fastq.gz	Fastqsanger.gz

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RNA-seq of primary mouse monocytes from miR-150 knockout and Tet3 knockout mice compared to wild type controls

Project description:Monocytes were isolated from blood of Wildtype, Mir150 and TET3 knockout mice, sorted for classical and non-classical monocyte subsets. RNA seq was performed on unstimulated monocytes.

2018-10-26 | E-MTAB-7291 | biostudies-arrayexpress

Transcriptome profiling of left ventricles from cardiac-specific miR-150 conditional knockout mice

Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from cardiac-specific miR-150 conditional knockout KO (cKO) mice were performed to identify novel miR-150 targets in the heart.

2021-08-18 | GSE177057 | GEO

Tet3 regulates terminal cell differentiation at the metabolic level

Project description:To define TET3 function in cell differentiation, we profiled the intestinal epithelium at the single-cell level from wild-type and Tet3 knockout mice. Our works shows that, in the absence of TET3, enterocytes exhibit an aberrant differentiation trajectory and do not acquire a physiological cell identity due to an impairment in oxidative phosphorylation, specifically due to the reduced expression of genes encoding for ATP synthase membrane domain subunits. To assess whether the downregulation of ATP synthase subunits upon TET3 loss was due to a TET3 catalytic or non-catalytic activity, we examined global DNA methylation patterns in wild-type and Tet3 knockout intestinal epithelium by whole-genome bisulfite sequencing (WGBS). Our results show that these critical ATP synthase subunits coding-genes did not show any hyperDMR in their regulatory regions, excluding TET3 catalytic activity as the mechanism underlying their decreased gene expression and, pointing thus to TET3 non-catalytic activity.

2024-10-22 | GSE274671 | GEO

E-MTAB-7291

Project description:RNA-seq of primary mouse monocytes from miR-150 knockout and Tet3 knockout mice compared to wild type controls

2019-01-16 | E-MTAB-7291 | ExpressionAtlas

Rest recruits neuronal Tet3 to induce chromatin remodeling and gene expression

Project description:Ten-eleven translocation (Tet) hydroxylases (Tet1-3) oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). In neurons increased 5hmC levels within gene bodies correlate positively with gene expression. The mechanisms controlling Tet activity and 5hmC levels are poorly understood. In particular, it is not known how the neuronal Tet3 isoform lacking a DNA binding domain is targeted to the DNA. To identify factors binding to Tet3 we screened for proteins that co-precipitate with Tet3 from mouse retina and identified the transcriptional repressor Rest as a highly enriched Tet3-specific interactor. Rest was able to enhance Tet3 hydroxylase activity after co-expression and overexpression of Tet3 activated transcription of Rest-target genes. Moreover, we found that Tet3 also interacts with Nsd3 and two other H3K36 methyltransferases and is able to induce H3K36 trimethylation. We propose a mechanism for transcriptional activation in neurons that involves Rest-guided targeting of Tet3 to the DNA for directed 5hmC-generation and Nsd3-mediated H3K36 trimethylation.

2015-04-02 | PXD001857 | Pride

Effects of TET3 deletion on gene expression in ileum [RNA-seq]

Project description:Bulk RNA-seq show differential gene expression profile beween Wild type (WT) and Tet3 knockout (KO) in ileum. We identified genes involved in innate immune defense, anti-microbial response and growth signaling to be affected by TET3 deletion.

2023-09-04 | GSE241790 | GEO

Redirected nuclear glutamate dehydrogenase supplies Tet3 with a-ketoglutarate in neurons

Project description:Tet3 is an Fe2+-dependent enzyme that oxidizes genomic 5-methylcytosine to 5-hydroxymethylcytosine with the help of alpha-ketoglutarate and oxygen. It is the most abundant Tet enzyme in differentiated tissues including brain. Adult brain contains the highest 5-hydroxymethylcytosine levels. How alpha-ketoglutarate is made available for the oxidation of mC in brain cells and how the Tet activity is linked to neural activity are unsolved questions. Our experiments with full mouse brains show that Tet3 interacts in the nucleus directly with selected enzymes of the mitochondrial citric acid cycle. This leads to the formation of isocitrate. Tet3 also interacts with aspartate aminotransferase, which produces oxaloacetate. Although oxaloacetate and isocitrate are biosynthetic alpha-ketoglutarate precursors, they function as inhibitors of Tet3 and are needed to protect the reactive Fe2+ center from degrading DNA. The supply of Tet3 with alpha-ketoglutarate is established by a direct interaction of Tet3 with glutamate dehydrogenase (Glud1), which converts the neurotransmitter glutamate directly into alpha-ketoglutarate. This links Tet3 function to neural activity.

2021-05-10 | PXD004518 | Pride

Haploinsufficiency, but not defective paternal 5mC oxidation, accounts for the developmental defects of maternal Tet3 knockouts

Project description:DNA demethylation of paternal genome in zygotes takes place in various mammals including mice and human. Recent studies have revealed that this is achieved through Tet3-mediated iterative oxidation of 5-methylcytosine (5mC) coupled with replication-dependent dilution. Tet3-mediated paternal DNA demethylation is believed to be required for mouse development given that Tet3 heterozygous embryos, derived by fertilizing Tet3 knockout (KO) oocytes with wild-type (WT) sperms, exhibit 5mC oxidation defects and embryonic sublethality, Here we demonstrate that the sublethality phenotype of the maternal KO mice is caused by haploinsufficiency of Tet3, but not by defective paternal 5mC oxidation. We found that Tet3 heterozygous mice derived from crosses of heterozygous father or mother with WT mice also exhibit sublethality phenotype similarly to Tet3 maternal KO mice. Importantly, embryos reconstituted with WT paternal nuclei that bypassed 5mC oxidation develop to term and grow to adulthood normally. Genome-scale DNA methylation analysis of the maternal KO zygotes and blastocysts demonstrated that hypermethylation caused by the depletion of maternal Tet3 is largely diminished by the blastocyst stage. Our study thus not only demonstrates that Tet3-mediated paternal 5mC oxidation is dispensable for mouse development but also suggests the existence of a compensation mechanism in preimplantation embryos that can compensate for the defective 5mC oxidation in zygotes. This data set includes RRBS data of wild-type and maternal Tet3 KO zygotes and blastocysts (C57BL/6J x CAST/EiJ)

2015-02-28 | E-GEOD-62719 | biostudies-arrayexpress

Expression profiling on lactation day 2 mammary epithelial cells from constitutive miR-150 expressing mice compared to controls.

Project description:Constitutive expression of miR-150 in mammary epithelium causes severe lactation defects. Mammary epithelial cells (MECs) at lactation day 2 were isolated from four homozygous ROSA26-lox-STOP-lox-miR-150 (Stop-150) mice with WAP-driven Cre (WAP-Cre) and compared to MECs from four WAP-Cre control mice. Statistical analysis of the mRNA changes between the two genotypes identified supression of many lipid and cholesterol synthesis genes due to constitutive expression of miR-150.

2016-10-01 | GSE80666 | GEO

Effect of TET1 and TET3 overexpression on the transcriptome of HEK293 cells

Project description:We compared TET1 and TET3 overexpressing cells to uninduced cells with endogenous levels of the respective transcript to determine global gene expression changes. TET1 overexpression, TET3 overexpression

2015-07-16 | E-GEOD-39186 | biostudies-arrayexpress

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