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TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions

ABSTRACT: TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions

PROVIDER: PRJNA641866 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12090700.fastq.gz	Fastqsanger.gz
	SRR12090800.fastq.gz	Fastqsanger.gz
	SRR12090900.fastq.gz	Fastqsanger.gz
	SRR12091000.fastq.gz	Fastqsanger.gz
	SRR12091100.fastq.gz	Fastqsanger.gz

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TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions

Project description:Estrogen receptor-alpha (ER) drives tumour development and metastasis in ER positive (ER+) breast cancer. GATA3 is a transcription factor that has been closely linked to ER function, but the role of GATA3 in ER-transcriptional activity is not clear. We sought to identify the contribution of GATA3 to the ER complex, by conducting quantitative multiplexed rapid immunoprecipitation mass spectrometry of endogenous proteins (qPLEX-RIME), to assess changes to the ER complex in response to GATA3 depletion. Unexpectedly, very few proteins were dissociated from the ER complex in the absence of GATA3, with the only major change being loss of TET2 in the ER complex. In breast cancer cells and Patient-Derived Xenograft (PDX) tissue, TET2 binding events were shown to constitute a near-total subset of ER binding events, and loss of TET2 was functionally associated with reduced activation of proliferative pathways. To investigate the TET2-ER relationship, the role of TET2 in regulating DNA modifications in ER+ breast cancer cells was examined. TET2 knockdown did not appear to result in changes to global DNA methylation, however, oxidation of methylated DNA to 5-hydroxymethylcytosine (5hmC) was significantly reduced after TET2 depletion and these events occurred at ER enhancers. These findings implicate TET2 in the production and maintenance of 5hmC at ER sites, providing a potential mechanism for TET2-mediated regulation of ER target genes.

2021-02-10 | PXD019438 | Pride

TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [MMS/RRHP]

Project description:TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [MMS/RRHP]

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TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [ChIP-Seq]

Project description:TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [ChIP-Seq]

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TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [RNA-Seq]

Project description:TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [RNA-Seq]

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TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [RNA-Seq]

Project description:Estrogen receptor-a (ER) drives tumour development and metastasis in ER positive (ER+) breast cancer. GATA3 is a transcription factor that has been closely linked to ER function, but the role of GATA3 in ER transcriptional activity is not clear. We sought to identify the contribution of GATA3 to the ER complex by conducting quantitative multiplexed rapid immunoprecipitation mass spectrometry of endogenous proteins (qPLEX-RIME) to assess changes to the ER complex in response to GATA3 depletion. Unexpectedly, very few proteins were dissociated from the ER complex in the absence of GATA3, with the only major change being depletion of TET2 from the ER complex. In breast cancer cells and Patient-Derived Xenograft (PDX) tissue, TET2 binding events were shown to constitute a near-total subset of ER binding events, and loss of TET2 was functionally associated with reduced activation of proliferative pathways. To investigate the TET2-ER relationship, the role of TET2 in regulating DNA modifications in ER+ breast cancer cells was examined. TET2 knockdown did not appear to result in changes to global DNA methylation, however, oxidation of methylated DNA to 5-hydroxymethylcytosine (5hmC) was significantly reduced after TET2 depletion and these events occurred at ER enhancers. These findings implicate TET2 in the production and maintenance of 5hmC at ER sites, providing a potential mechanism for TET2-mediated regulation of ER target genes.

2021-02-10 | GSE153250 | GEO

TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [MMS/RRHP]

2021-02-10 | GSE153252 | GEO

TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [ChIP-Seq]

2021-02-10 | GSE153251 | GEO

Methylome of 5mC and 5hmC regulated by NEIL2

Project description:To elucidate the role of DNA glycosylase NEIL2 in regulation of DNA methylome, we performed genome sequencing of epigenetic marker 5mC and 5hmC in genome-wide using enyme-based library methods of TAPS and CAPS. The 5mC and 5hmC profile in CpG contect was further extracted and analysed.

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TET2 is a component of the estrogen receptor complex and controls 5mC to 5hmC conversion at estrogen receptor cis-regulatory regions.

Project description:Estrogen receptor-α (ER) drives tumor development in ER-positive (ER+) breast cancer. The transcription factor GATA3 has been closely linked to ER function, but its precise role in this setting remains unclear. Quantitative proteomics was used to assess changes to the ER complex in response to GATA3 depletion. Unexpectedly, few proteins were lost from the ER complex in the absence of GATA3, with the only major change being depletion of the dioxygenase TET2. TET2 binding constituted a near-total subset of ER binding in multiple breast cancer models, with loss of TET2 associated with reduced activation of proliferative pathways. TET2 knockdown did not appear to change global methylated cytosine (5mC) levels; however, oxidation of 5mC to 5-hydroxymethylcytosine (5hmC) was significantly reduced, and these events occurred at ER enhancers. These findings implicate TET2 in the maintenance of 5hmC at ER sites, providing a potential mechanism for TET2-mediated regulation of ER target genes.

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Direct, bisulfite-free 5mC and 5hmC sequencing at single-cell resolution

Project description:We report the first direct sequencing methodologies, termed scTAPS and scCAPS+ (exclusive to 5hmC), which enable quantitative detection of 5mC and 5hmC at single-base resolution and single-cell level. With ~90% mapping efficacy, our methods accurately benchmark 5mC and 5hmC profiles in CD8+ T and mES cells, respectively. Notably, scCAPS+ revealed a global increase in 5hmC within the hippocampus of aging mice, particularly evident in non-neurons.

2025-07-18 | GSE255771 | GEO

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