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Genome-wide maps of 5hmC in control and Tet3 inactivated lung smooth muscle cells

ABSTRACT: Genome-wide maps of 5hmC in control and Tet3 inactivated lung smooth muscle cells

PROVIDER: PRJNA702087 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13720925.fastq.gz	Fastqsanger.gz
	SRR13720926.fastq.gz	Fastqsanger.gz
	SRR13720927.fastq.gz	Fastqsanger.gz
	SRR13720928.fastq.gz	Fastqsanger.gz
	SRR13720929.fastq.gz	Fastqsanger.gz

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Genome-wide maps of 5hmC in control and Tet3 inactivated lung smooth muscle cells

Project description:To examine the influences for 5hmC enrichment on genome wide after Tet3 inactivation, we determined the enrichment profiles of 5hmC, the direct demethylated target of Tet3, by hMeDIP-seq with genomic DNA from control and Tet3 inactivated lung smooth muscle cells

2021-04-30 | GSE166830 | GEO

Genome-wide maps of 5hmC in control and Tet3 inactivated lung smooth muscle cells.

Project description:To examine the influences for 5hmC enrichment on genome wide after Tet3 inactivation, we determined the enrichment profiles of 5hmC, the direct demethylated target of Tet3, by Nano-hmC-seq with genomic DNA from control and Tet3 inactivated lung smooth muscle cells

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Genome-wide maps of 5hmC in control and Tet3 inactivated lung smooth muscle cells.

Project description:Genome-wide maps of 5hmC in control and Tet3 inactivated lung smooth muscle cells.

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Genome-wide maps of Cap signal in control and Tet3 inactivated lung smooth muscle cells

Project description:To examine the initiation cap signal after Tet3 inactivation, we performed the Cap analysis gene expression (CAGE) sequencing with total RNA from control and Tet3 inactivated lung smooth muscle cells.

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Genome-wide maps of Cap signal in control and Tet3 inactivated lung smooth muscle cells

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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

Loss of TET3-mediated 5hmC promotes the Neurodegeneration of Alzheimer’s disease

Project description:Alzheimer's disease (AD) was attributed to alterations in multiple epigenetic systems including DNA methylation and demethylation patterns. DNA 5-hydroxymethylcytosin (5hmC), an epigenetic hallmark, plays importantly regulatory role in many biological processes. However, the 5hmC-mediated epigenetic underpinnings of AD neurodegeneration remain poorly understood. Here we report that selective loss of 5hmC is substantially presented in human AD and 3xTg-AD mouse neocortical and hippocampal neurons. Quantitative genome-wide analysis of hMeDIP-seq reveals that neuron-specific shift in decreased 5hmC enrichment in regions of promoter, intergenic and gene body of mRNA and lncRNA genes was found in3xTg-AD mice. We further identified that TET3, an enzyme that converts 5-methylcytosine (5mC) to 5hmC, responded to Beta amyloid neuronal toxicity and was mainly responsible for loss of 5hmC in AD brain. Overexpression of human TET3 catalytic domain (hTET3CD) significantly improves the neuroinflammation, neuropathological progression and cognitive deficits in 3xTg-AD mice. These findings implicate as a potential hallmark, TET3-mediated 5hmC epigenetic dysregulation is involved in driving AD neurodegeneration.

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Project description:Tet3 was deleted in smooth muscle cells by tamoxifen-induced Cre-recombination in 8 weeks old mice. Laser-capture microdissection was used to isolate bronchiolar or vascular tissue from lung sections of 16 weeks old mice for transcriptome analysis.

2022-09-19 | E-MTAB-10144 | biostudies-arrayexpress

Methylation arrays elucidate 5mC and 5hmC levels of human glioblastoma cell line LN229 upon restoration of TET3 expression.

Project description:DNA hydroxymethylation is frequently lost in glioblastoma. We hypothesized that reduced 5hmC levels might be related to the impaired expression of TET proteins in brain tumors. In this study we performed a genome-wide methylation analysis of LN229 cells stably transfected with scramble or TET3 overexpressing vectors. TET3 overexpression partially restored the genome-wide patterns of 5hmC characteristic of control brain samples in glioblastoma cell lines.

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Circadian clock regulator Bmal1 gates axon regeneration via Tet3-5hmC mediated epigenetics

Project description:Axon regeneration of dorsal root ganglia (DRG) neurons after peripheral axotomy involves epigenetic reconfigurations that rewire gene regulatory circuits to establish regenerative gene program. However, the mechanisms and transcriptional regulators remain poorly understood. Here, we conducted an unbiased survey of DNA differentially hydroxymethylated regions (DhMRs) in DRG after peripheral lesion, which identified enriched binding motif for Bmal1, a transcription factor and a central regulator of the circadian clock. Through applying conditional deletion of Bmal1, in vitro and in vivo models of axon regrowth, and transcriptomic profiling, we showed that Bmal1 inhibits axon regeneration in part through Tet3-dependent manner. Mechanistically, Bmal1 functions as a gatekeeper of neuroepigenetic injury responses by limiting Tet3 expression and restricting 5hmC modifications. Notably, Bmal1-regulated genes after axotomy not only concern axon guidance and axon regrowth, but also stress responses, energy homeostasis, and neuroinflammation. Furthermore, we uncovered diurnal oscillation of Tet3 and 5hmC in DRG neurons, and this epigenetic rhythm corresponded to time-of-day effect on axon growth potential. Collectively, our studies showed that Bmal1 deletion mimics the conditioning lesion in lifting epigenetic barriers to enhance axon regeneration.

2023-08-02 | GSE233367 | GEO

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