E-MTAB-3194
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-3194 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-3194-analysis-methods.tsv | Tabular | |||
| E-MTAB-3194-analytics.tsv | Tabular | |||
| E-MTAB-3194-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-3194-configuration.xml | Xml | |||
| E-MTAB-3194-g1_g2-mvaPlot.png | Other |
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Project description:A dynamic switch of Ezh1 isoforms controls PRC2 mediated adaptive epigenetic response in post-mitotic cells
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Project description:Circadian rhythmicity of gene expression is a conserved feature of cell physiology. This involves fine tuning between transcriptional and post-transcriptional molecular mechanisms, strongly dependent on the metabolic state of the cell, which guarantees adaptive plasticity of tissue-specific genetic programs. Dynamics of epigenome structure and epigenetic regulators support this plasticity. However, the intermingle between epigenome and RNA Pol II rhythmicity remains to be investigated. Here we identify the Polycomb group (PcG) protein EZH1 as a gateway bridging function regulating periodic alternation between chromatin mediated silencing and active transcription in post-mitotic skeletal muscle cells. We show that PRC2-EZH1 core components are under direct regulation of BMAL1, and show an oscillatory behavior and a regulated periodic assembly of PRC2-EZH1 complex. Instead at alternate Zeitgeber points, EZH1 becomes essential for circadian gene expression, through stabilization of RNA Pol II preinitiation complex controlling nascent transcription process. Collectively, our data show that EZH1 depending on the stoichiometry of its partners guarantees both negative and positive modulation of RNA Pol II activity, resulting in oscillatory transcription.
2024-10-11 | PXD035453 | Pride
Project description:A cytosolic Ezh1 isoform modulates PRC2-Ezh1 repressive function as adaptive epigenetic response in post-mitotic cells
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Project description:Polycomb Repressive Complex 2 (PRC2) plays crucial roles in transcriptional regulation and stem cell development. However, the context-specific functions associated with alternative subunits remain largely unexplored. Here we show that the related enzymatic subunits EZH1 and EZH2 undergo an expression switch during hematopoiesis. We examine the in vivo stoichiometry of the PRC2 complexes by quantitative proteomics and reveal the existence of an EZH1-SUZ12 sub-complex lacking EED. We provide evidence that EZH1 together with SUZ12 form a non-canonical PRC2 complex, occupy active chromatin domains in the absence of H3K27me3, and positively regulate gene expression. Loss of EZH2 expression leads to global repositioning of EZH1 chromatin occupancy to EZH2 targets. Moreover, we demonstrate that an erythroid-specific enhancer mediates transcriptional activation of EZH1, and a switch from GATA2 to GATA1 controls the developmental EZH1/2 switch by differential association with EZH1 enhancers during erythropoiesis. Thus, the lineage- and developmental stage-specific regulation of PRC2 expression and subunit composition leads to a switch from canonical silencing to non-canonical PRC2 functions during blood stem cell specification. Analysis of genomic occupancy of EZH1, EZH2, EED, SUZ12, various histone marks and transcription factors in primary human fetal liver proerythroblasts by ChIP-seq. Sample GSM970262 was used as the input DNA sample.
2015-01-01 | E-GEOD-59087 | biostudies-arrayexpress
Project description:Polycomb Repressive Complex 2 (PRC2) plays crucial roles in transcriptional regulation and stem cell development. However, the context-specific functions associated with alternative subunits remain largely unexplored. Here we show that the related enzymatic subunits EZH1 and EZH2 undergo an expression switch during hematopoiesis. We examine the in vivo stoichiometry of the PRC2 complexes by quantitative proteomics and reveal the existence of an EZH1-SUZ12 sub-complex lacking EED. We provide evidence that EZH1 together with SUZ12 form a non-canonical PRC2 complex, occupy active chromatin domains in the absence of H3K27me3, and positively regulate gene expression. Loss of EZH2 expression leads to global repositioning of EZH1 chromatin occupancy to EZH2 targets. Moreover, we demonstrate that an erythroid-specific enhancer mediates transcriptional activation of EZH1, and a switch from GATA2 to GATA1 controls the developmental EZH1/2 switch by differential association with EZH1 enhancers during erythropoiesis. Thus, the lineage- and developmental stage-specific regulation of PRC2 expression and subunit composition leads to a switch from canonical silencing to non-canonical PRC2 functions during blood stem cell specification. Transcriptional profiling in primary human fetal liver proerythroblasts upon lentiviral shRNA-mediated knockdown of EZH1, EZH2, EED, or SUZ12 by RNA-seq analysis.
2015-01-01 | E-GEOD-59089 | biostudies-arrayexpress
Project description:Polycomb Repressive Complex 2 (PRC2) plays crucial roles in transcriptional regulation and stem cell development. However, the context-specific functions associated with alternative subunits remain largely unexplored. Here we show that the related enzymatic subunits EZH1 and EZH2 undergo an expression switch during hematopoiesis. We examine the in vivo stoichiometry of the PRC2 complexes by quantitative proteomics and reveal the existence of an EZH1-SUZ12 sub-complex lacking EED. We provide evidence that EZH1 together with SUZ12 form a non-canonical PRC2 complex, occupy active chromatin domains in the absence of H3K27me3, and positively regulate gene expression. Loss of EZH2 expression leads to global repositioning of EZH1 chromatin occupancy to EZH2 targets. Moreover, we demonstrate that an erythroid-specific enhancer mediates transcriptional activation of EZH1, and a switch from GATA2 to GATA1 controls the developmental EZH1/2 switch by differential association with EZH1 enhancers during erythropoiesis. Thus, the lineage- and developmental stage-specific regulation of PRC2 expression and subunit composition leads to a switch from canonical silencing to non-canonical PRC2 functions during blood stem cell specification.
2015-01-01 | GSE59089 | GEO
Project description:Polycomb Repressive Complex 2 (PRC2) plays crucial roles in transcriptional regulation and stem cell development. However, the context-specific functions associated with alternative subunits remain largely unexplored. Here we show that the related enzymatic subunits EZH1 and EZH2 undergo an expression switch during hematopoiesis. We examine the in vivo stoichiometry of the PRC2 complexes by quantitative proteomics and reveal the existence of an EZH1-SUZ12 sub-complex lacking EED. We provide evidence that EZH1 together with SUZ12 form a non-canonical PRC2 complex, occupy active chromatin domains in the absence of H3K27me3, and positively regulate gene expression. Loss of EZH2 expression leads to global repositioning of EZH1 chromatin occupancy to EZH2 targets. Moreover, we demonstrate that an erythroid-specific enhancer mediates transcriptional activation of EZH1, and a switch from GATA2 to GATA1 controls the developmental EZH1/2 switch by differential association with EZH1 enhancers during erythropoiesis. Thus, the lineage- and developmental stage-specific regulation of PRC2 expression and subunit composition leads to a switch from canonical silencing to non-canonical PRC2 functions during blood stem cell specification.
2015-01-01 | GSE59087 | GEO
Project description:Circadian rhythmicity of gene expression is a conserved feature of cell physiology. This involves the fine tuning between transcriptional and post-transcriptional molecular mechanisms, strongly dependent on the metabolic state of the cell that guarantees intrinsic plasticity of tissue specific genetic programs. To support the plastic properties a key role is played by the dynamics of epigenome structure and its regulators. Here we investigate the role of the Polycomb cell memory complex PRC2-EZH1 in regulating transcriptional rhythmicity in post-mitotic skeletal muscle cells. We show that PRC2-EZH1 core components are under direct regulation of BMAL1, show an oscillatory behavior and control both silencing and activation of target genes. Fully assembled PRC2-EZH1 complex negatively regulates cyclic expression of direct targets through modulation of cyclic H3K27me3 status. Conversely, we show that EZH1 regulates constitutive circadian genes expression, through stabilization of RNA Pol II machinery and maintenance of transcription process fidelity. Collectively, these findings unveil the dual and multi role of PcG in circadian gene regulation in adult skeletal muscle cells, and the plastic nature of PcG cell memory system in somatic cells.
2025-01-03 | GSE198409 | GEO
Project description:Polycomb proteins assemble to form complexes with important roles in epigenetic regulation. The Polycomb Repressive Complex 2 (PRC2) modulates the di- and tri-methylation of lysine 27 on histone H3, each of which are associated with gene repression. Although three subunits, EZH1/2, SUZ12 and EED, form the catalytic core of PRC2, a wider group of proteins associate with low stoichiometry. This raises the question of whether dynamic variation of the PRC2 interactome results in alternative forms of the complex during differentiation. Here we compared the physical interactions of PRC2 in undifferentiated and differentiated states of NTERA2 pluripotent embryonic carcinoma cells. Label-free quantitative proteomics was used to assess endogenous immunoprecipitation of the EZH2 and SUZ12 subunits of PRC2. A high stringency dataset reflecting the endogenous state of PRC2 was produced that included all previously reported ‘core’ and ‘associated’ PRC2 components, and several novel interacting proteins. Comparison of the interactomes obtained in undifferentiated and differentiated cells revealed candidate proteins that favoured either one or other state. For example, SALL4 and ZNF281 associate with PRC2 in pluripotent cells, while PCL1 and SMAD3 more associate with PRC2 in differentiating cells. Analysis of the mRNA and protein levels of these factors found that their association with PRC2 correlated with their cell state-specific expression. Taken together, we propose that dynamic changes to the PRC2 interactome during differentiation may contribute to directing its activity during cell fate transitions.
2016-09-27 | PXD004462 | Pride
Project description:Trimethylation on H3K27 (H3K27me3) mediated by Polycomb repressive complex 2 (PRC2) has been linked to embryonic stem cell (ESC) identity and pluripotency. EZH2, the catalytic subunit of PRC2, has been reported as the sole histone methyltransferase that methylates H3K27 and mediates transcriptional silencing. Analysis of Ezh2(-/-) ESCs suggests existence of an additional enzyme(s) catalyzing H3K27 methylation. We have identified EZH1, a homolog of EZH2 that is physically present in a noncanonical PRC2 complex, as an H3K27 methyltransferase in vivo and in vitro. EZH1 colocalizes with the H3K27me3 mark on chromatin and preferentially preserves this mark on development-related genes in Ezh2(-/-) ESCs. Depletion of Ezh1 in cells lacking Ezh2 abolishes residual methylation on H3K27 and derepresses H3K27me3 target genes, demonstrating a role of EZH1 in safeguarding ESC identity. Ezh1 partially complements Ezh2 in executing pluripotency during ESC differentiation, suggesting that cell-fate transitions require epigenetic specificity.
2009-03-25 | GSE15388 | GEO