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A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [ChIRP-Seq]

ABSTRACT: A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [ChIRP-Seq]

PROVIDER: PRJNA819087 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18456000_1.fastq.gz	Fastqsanger.gz
	SRR18456000_2.fastq.gz	Fastqsanger.gz
	SRR18456001_1.fastq.gz	Fastqsanger.gz
	SRR18456001_2.fastq.gz	Fastqsanger.gz
	SRR18456002_1.fastq.gz	Fastqsanger.gz

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A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [ChIRP-Seq]

Project description:The mammalian Ten-eleven translocation (TET) family proteins regulate the epigenome through catalytic activity (CA)-dependent and -independent functions. While catalytic activity of TETs has been intensely studied as DNA demethylation enzymes, little is known about their CA-independent function in early embryo development. Here we defined the CA-independent function of TET1 in naïve-to-formative pluripotent states transition. Using a proteomics method, we mapped the TET1 interactome and identified Paraspeckle component 1 (PSPC1) as a partner of TET1 for transcriptional repression at the bivalent genes in early development. Genome-wide location analysis revealed that PSPC1-bound regions largely overlap with TET1 and Polycomb repressive complex 2 (PRC2) subunits. Functional studies with genetic methods indicated that PSPC1 and TET1 repress, while lncRNA Neat1 activates the bivalent genes during their transcriptional activation. In embryonic stem cell (ESC) state, Neat1 tethers TET1, PSPC1, and PRC2 at promoters. During the ESCs to formative Epiblast like stem cells (EpiLCs) differentiation, PSPC1 and TET1 repress the PRC2 affinity to nascent mRNA transcripts of bivalent genes, while Neat1 facilitates PRC2 binding to those transcripts. Our study reveals a molecular mechanism by which proteins TET1 and PSPC1, and lncRNA Neat1 dynamically regulate gene transcription by modulating the PRC2 activity in pluripotent states transition.

2022-06-07 | GSE199265 | GEO

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [ChIP-seq]

2022-06-07 | GSE182442 | GEO

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [RNA-seq]

2022-06-07 | GSE182441 | GEO

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [H3 ChIP-Seq]

2022-06-07 | GSE199266 | GEO

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency

Project description:A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency

| PRJNA756267 | ENA

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [RNA-seq]

Project description:A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [RNA-seq]

| PRJNA756269 | ENA

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [ChIP-seq]

Project description:A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [ChIP-seq]

| PRJNA756270 | ENA

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [H3 ChIP-Seq]

Project description:A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [H3 ChIP-Seq]

| PRJNA819086 | ENA

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency.

Project description:TET1 maintains hypomethylation at bivalent promoters through its catalytic activity in embryonic stem cells (ESCs). However, TET1 catalytic activity-independent function in regulating bivalent genes is not well understood. Using a proteomics approach, we map the TET1 interactome in ESCs and identify PSPC1 as a TET1 partner. Genome-wide location analysis reveals that PSPC1 functionally associates with TET1 and Polycomb repressive complex-2 (PRC2). We establish that PSPC1 and TET1 repress, and the lncRNA Neat1 activates, bivalent gene expression. In ESCs, Neat1 is preferentially bound to PSPC1 alongside its PRC2 association at bivalent promoters. During the ESC-to-epiblast-like stem cell (EpiLC) transition, PSPC1 and TET1 maintain PRC2 chromatin occupancy at bivalent gene promoters, while Neat1 facilitates the activation of certain bivalent genes by promoting PRC2 binding to their mRNAs. Our study demonstrates a TET1-PSPC1-Neat1 molecular axis that modulates PRC2-binding affinity to chromatin and bivalent gene transcripts in controlling stem cell bivalency.

| S-EPMC9214724 | biostudies-literature

The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [ChIRP-seq]

Project description:The transcription factor ΔNp63, a master regulator of epithelial biology, is involved in regulating epithelial stem cell function and maintaining the integrity of stratified epithelial tissues such as the epidermis. To this end, ΔNp63 acts as transcriptional repressor or activator towards a distinct subset of protein-coding genes and microRNAs. However, how and whether ∆Np63 regulates long non-coding RNA (lncRNAs) expression is not known. Here, we identified the lncRNAs NEAT1 and MALAT1 as a bona fide ΔNp63 transcriptional targets. We found that in proliferating human keratinocytes ∆Np63 represses NEAT1 and MALAT1 expression by recruiting the histone deacetylates HDAC1/HDAC2 to the p63 DNA binding site located in the proximal promoter of NEAT1 and MALAT1 genomic loci. Upon induction of differentiation, ∆Np63 down-regulation is associated by a marked increase of NEAT1 RNA levels, resulting in an increased assembly of paraspeckles foci both in vitro and in human skin tissues. RNA-seq analysis associated with global DNA binding profile (ChIRP-seq) revealed that NEAT1 associates with the promoter of key epithelial transcription factors sustaining their expression during epidermal differentiation. These molecular events might explain the inability of NEAT1-depleted keratinocytes to undergo the correct epidermal differentiation program. Remarkably, NEAT1 expression is dysregulated in those skin pathologies characterized by aberrant keratinocytes differentiation such as ichthyosis and psoriasis, suggesting its potential involvement in the pathogenesis of skin disorders.

2023-05-17 | GSE205959 | GEO

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