Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243882 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1220293.fastq.gz | Fastqsanger.gz | |||
| SRR1220294.fastq.gz | Fastqsanger.gz | |||
| SRR1220295.fastq.gz | Fastqsanger.gz | |||
| SRR646464.fastq.gz | Fastqsanger.gz | |||
| SRR646465.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptional activation without chromatin marking in developmentally regulated genes [ChIP-seq]
| PRJNA210868 | ENA
Project description:We demonstrate that chromodomain helicase DNA-binding domain 2 (Chd2) is required to maintain the differentiation potential of mouse ESCs. Chd2-depleted ESCs showed suppressed expression of developmentally regulated genes upon differentiation and subsequent differentiation defects without affecting gene expression in the undifferentiated state. Furthermore, chromatin immunoprecipitation followed by sequencing revealed alterations in a proportion of nucleosomes of developmentally regulated genes in Chd2-depleted ESCs to enhance histone variant H3.3 enrichment, leading to elevated trimethylation of histone H3 lysine 27.Chd2 is essential to prevent suppressive chromatin formation in developmentally regulated genes and determines subsequent effects on developmental processes in the undifferentiated state.
2017-05-15 | GSE96660 | GEO
Project description:We demonstrate that chromodomain helicase DNA-binding domain 2 (Chd2) is required to maintain the differentiation potential of mouse ESCs. Chd2-depleted ESCs showed suppressed expression of developmentally regulated genes upon differentiation and subsequent differentiation defects without affecting gene expression in the undifferentiated state. Furthermore, chromatin immunoprecipitation followed by sequencing revealed alterations in a proportion of nucleosomes of developmentally regulated genes in Chd2-depleted ESCs to enhance histone variant H3.3 enrichment, leading to elevated trimethylation of histone H3 lysine 27.Chd2 is essential to prevent suppressive chromatin formation in developmentally regulated genes and determines subsequent effects on developmental processes in the undifferentiated state.
2017-05-15 | GSE96661 | GEO
Project description:Promoters of many developmentally regulated genes, in the embryonic stem cell state, have a bivalent mark of H3K27me3 and H3K4me3, proposed to confer precise temporal activation upon differentiation. Although Polycomb repressive complex 2 is known to implement H3K27 trimethylation, the COMPASS family member responsible for H3K4me3 at bivalently marked promoters was previously unknown. Here, we identify Mll2 (KMT2b) as the enzyme catalyzing H3K4 trimethylation at bivalently marked promoters in embryonic stem cells. Although H3K4me3 at bivalent genes is proposed to prime future activation, we detected no substantial defect in rapid transcriptional induction after retinoic acid treatment in Mll2-depleted cells. Our identification of the Mll2 complex as the COMPASS family member responsible for H3K4me3 marking at bivalent promoters provides an opportunity to reevaluate and experimentally test models for the function of bivalency in the embryonic stem cell state and in differentiation.
2013-08-11 | GSE48172 | GEO
Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns. To determine NFATc1-regulated genes, a total of 5 samples were derived from human umbilical vein endothelial cells (HUVECs) stimulated with or without 50ng/mL VEGF (VEGF 60min and 0min, respectively), pretreated with cyclosporine A (VEGF 60min plus CsA) and infected with adenovirus expressing the control or constitutively active NFATc1 (Ad-control and Ad-NFATc1).
2013-09-01 | E-GEOD-49426 | biostudies-arrayexpress
Project description:Transcriptional regulation of developmentally controlled genes is at the heart of differentiation and organogenesis. In this study, we have performed global genomic analyses in murine embryonic stem (ES) cells and in human cells in response to activation signals. We have identified an essential role for the ELL/P-TEFbcontaining Super Elongation Complex (SEC) in the regulation of gene expression including several genes bearing paused RNA polymerase II (Pol II). Paused Pol II has been proposed to be associated with loci that respond rapidly to environmental stimuli. However, our studies in ES cells have also identified a requirement for SEC at genes without preloaded Pol II, which also respond dynamically to differentiation signals. Our findings suggest that SEC is a major class of active P-TEFb-containing complexes required for transcriptional activation in response to environmental cues such as differentiation signals. Examination of ELL2, AFF4, and Pol II before and after activation signals in two cell types.
2011-07-19 | E-GEOD-30267 | biostudies-arrayexpress
Project description:Promoters of many developmentally regulated genes, in the embryonic stem cell state, have a bivalent mark of H3K27me3 and H3K4me3, proposed to confer precise temporal activation upon differentiation. Although Polycomb repressive complex 2 is known to implement H3K27 trimethylation, the COMPASS family member responsible for H3K4me3 at bivalently marked promoters was previously unknown. Here, we identify Mll2 (KMT2b) as the enzyme catalyzing H3K4 trimethylation at bivalently marked promoters in embryonic stem cells. Although H3K4me3 at bivalent genes is proposed to prime future activation, we detected no substantial defect in rapid transcriptional induction after retinoic acid treatment in Mll2-depleted cells. Our identification of the Mll2 complex as the COMPASS family member responsible for H3K4me3 marking at bivalent promoters provides an opportunity to reevaluate and experimentally test models for the function of bivalency in the embryonic stem cell state and in differentiation. ChIP-Seq in mouse embryonic stem (mES) cells for MLL2. ChIP-seq of H3K4me1, H3K4me3 and H3K27me3 for mES cells with RNAi against MLL2(shMLL2) and control (shGFP). ChIP-seq of H3K4me3 in mES cells with RNAi against MLL3 (shMLL3). RNA-seq of mES cells with RNAi against MLL2 and control (shGFP). RNA-seq of control mES cells (shGFP) or MLL2 RNAi mES cells (shMLL2) induced with RA for 6h and 12h.
2013-08-11 | E-GEOD-48172 | biostudies-arrayexpress
Project description:BRD4 is a key regulatory factor in multiple cancers and cellular stress responses with pleotropic functions. BRD4 regulates chromatin remodeling and transcription through its histone acetyltransferase (HAT) and kinase activities, respectively. The mechanism responsible for switching BRD4 from a chromatin to transcriptional regulator is currently unknown. Here, we report that in response to a broad range of stimuli, this switch is mediated by the JNK kinase which directly interacts with BRD4. JNK specifically phosphorylates human BRD4 at Ser1117, Thr1186 and Thr1212, triggering transient BRD4 release from chromatin. JNK phosphorylation of BRD4 halts its HAT-mediated chromatin regulation and activates its transcription-enhancing kinase function. BRD4 release from chromatin is necessary to toggle between its enzymatic activities: chromatin-bound BRD4 is kinase inactive and RNA Pol II-bound BRD4 does not acetylate chromatin. BRD4 release from chromatin augments its interaction with and phosphorylation of key transcriptional regulators RNA Pol II, PTEFb and c-MYC. The PP4 phosphatase dephosphorylates JNK phosphorylated BRD4 in the nucleoplasm, which promotes its interaction with RNA Pol II at transcriptionally active sites. Accordingly, JNK-mediated release of BRD4 from chromatin leads to significantly elevated transcription of BRD4-regulated immune and inflammatory response genes through enhanced BRD4-Pol II interaction at the promoters of these genes. JNK phosphorylation of BRD4 occurs during T-cell activation and is required for epithelial to mesenchymal transition (EMT) in prostate cancer cells. These findings thus characterize a novel mechanism that triggers the transition of BRD4 from a chromatin regulator to transcriptional activator during stress/immune/inflammatory responses and EMT.
2024-01-16 | MSV000093873 | MassIVE
Project description:Enhancers play a central role in precisely regulating the spatiotemporal expression of developmentally regulated genes. The molecular mechanisms and factors required for controlling the inactive or poised enhancers and their function in future gene activation remain elusive. Here, we have identified that Ell3, a member of the Ell (Eleven-nineteen Lysine-rich Leukemia gene) family of RNA Pol II elongation factors, predominately occupies active and inactive enhancers of many developmentally regulated genes in mouse embryonic stem cells. Ell3 localizes to active enhancers of key stem cell renewal genes, but is not required for maintaining the undifferentiated state. Instead, Ell3 binding to inactive or poised enhancers is essential for marking them for stem cell specification through regulating the activation of key lineage-specific genes throughout differentiation. Ell3M-bM-^@M-^Ys association with enhancers is required for setting up proper Pol II occupancy at the proximal promoter regions of neighboring genes. This functional interaction between Ell3 and proximal promoter Pol II is dependent on cohesin. The depletion of cohesin subunits removes Ell3 from the enhancers and results in reduction in the levels of promoter proximally paused Pol II. Our study demonstrates that Ell3 is required for stem cell fate specification through regulating Pol II pausing on key developmental genes in the undifferentiated state and for their proper expression during differentiation. ChIP-seq of Ell3 in mES cells. ChIP-seq of Pol II in mES cells after Ell3 shRNA and non-targeting shRNA. RNA-seq of mES cells after Ell3 shRNA and non-targeting shRNA. RNA-seq of mouse embryoid bodies at day five after non-targeting shRNA.
2012-12-30 | E-GEOD-38148 | biostudies-arrayexpress
Project description:Enhancers play a central role in precisely regulating the spatiotemporal expression of developmentally regulated genes. The molecular mechanisms and factors required for controlling the inactive or poised enhancers and their function in future gene activation remain elusive. Here, we have identified that Ell3, a member of the Ell (Eleven-nineteen Lysine-rich Leukemia gene) family of RNA Pol II elongation factors, predominately occupies active and inactive enhancers of many developmentally regulated genes in mouse embryonic stem cells. Ell3 localizes to active enhancers of key stem cell renewal genes, but is not required for maintaining the undifferentiated state. Instead, Ell3 binding to inactive or poised enhancers is essential for marking them for stem cell specification through regulating the activation of key lineage-specific genes throughout differentiation. Ell3’s association with enhancers is required for setting up proper Pol II occupancy at the proximal promoter regions of neighboring genes. This functional interaction between Ell3 and proximal promoter Pol II is dependent on cohesin. The depletion of cohesin subunits removes Ell3 from the enhancers and results in reduction in the levels of promoter proximally paused Pol II. Our study demonstrates that Ell3 is required for stem cell fate specification through regulating Pol II pausing on key developmental genes in the undifferentiated state and for their proper expression during differentiation.
2012-12-30 | GSE38148 | GEO