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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE166830 | GEO | 2021/04/30

REPOSITORIES: GEO

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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 Nano-hmC-seq with genomic DNA from control and Tet3 inactivated lung smooth muscle cells

2022-09-21 | GSE202201 | GEO

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.

2019-02-19 | GSE126713 | GEO

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

| PRJNA702087 | ENA

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.

2021-04-01 | GSE168206 | GEO

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

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.

2018-03-03 | E-MTAB-6001 | biostudies-arrayexpress

Catalytic dependent and independent roles of Tet3 in activation of ectodermal and silencing of mesodermal programs during neuroectoderm specification

Project description:In this study: (1) we distinguished Tet3 target genes that are regulated by its catalytic vs. noncatalytic functions in neuroectoderm (NE) cells by transcriptomic profiling of Tet3 wildtype (WT), Tet3 catalytic mutant (Mut), and Tet3 knockout (KO) NE cells by RNA-seq. (2) We mapped genome-wide DNA methylation of Tet3-WT, Tet3-Mut, and Tet3-KO NE cells by WGBS. (3) We determined Tet3 genome-wide occupancy in Tet3-WT NE cells by CUT&Tag. (4) We mapped 5hmC rich regions in Tet3-WT, Tet3-Mut, and Tet3-KO NE cells by hmeDIP. (5) We overexpressed (OE) the Tet3 target gene Dnmt1 (D) or an empty vector (EV) in Tet3-WT, Tet3-Mut, and Tet3-KO NE cells and assessed gene expression by RNA-seq. (6) We overexpressed (OE) Tet3 (T) or an empty vector (EV) in Tet3-WT, Tet3-Mut, and Tet3-KO NE cells and examined gene expression changes in these cells by RNA-seq.

2024-04-02 | GSE237800 | GEO

Comparative high density microarray analysis of global 5hmC patterns in mouse brain and liver following independent affinity based enrichment protocols.

Project description:On mouse tiled microarrays (GPL17802), we profile 5hmC in WT mouse livers and brains following fragment enrichment by one of three affinity based techniques: i- antibody (HmeDIP), ii- Chemical capture (hMeSeal) and iii-JBP-1 protein affinity (JBP). HmeDIP and hMeSeal both return similar patterns of 5hmC whilst JBP enriched patterns (carriedo out on brain only) resemble background noise. 5hmC is largely found to reside in the bodies of active genes as well as being enriched over enhancer and promoter proximal regions. WT C57BL/6 mice aged 30-32 days old at time of organ removal. Tissues taken and frozen in liquid nitrogen prior to DNA extraction. Genomic DNA was sonicated (Bioruptor, Diagenode) to produce DNA fragments ranging in size from 200 to 1,000 bp, with a mean fragment size of around 300 bp. i- HmeDIP: antibody enrichment carried out as previously reported by Thomson et al 2013 (doi:10.1093/nar/gkt232). ii- HmeSeal: Enrichment based on the hMe-Seal based techniques described by Song et al 2010 (doi: 10.1038/nbt.1732) and marketed by Active motif under the name hydroxymethyl-collector kit. iii- JBP-1 affinity purification: Enrichment carried out using the Quest 5hmC DNA enrichment kit marketed by Zymo research.

2013-12-01 | E-GEOD-51577 | biostudies-arrayexpress

PGC7 and TET3 ChIP-seq results

Project description:PGC7 is a primordial germ cell (PGCs)-specific protein involved in epigenetic chromatin reprogramming in the zygote following fertilization. TET3 is a dioxygenase that catalyzes the conversion of the modified genomic base 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC) and plays a key role in epigenetic chromatin reprogramming in the zygote following fertilization. PGC7 participates in protection of DNA methylation in the maternal pronucleus by preventing conversion of 5mC to 5hmC by TET3 oxidization subsequent DNA demethylation. Thus we tested the co-localization of PGC7 and TET3 in specific loci by ChIP-seq assays.

2014-01-04 | E-GEOD-53809 | biostudies-arrayexpress

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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