Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-31234
PROVIDER: PRJNA146035 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE31233: Dynamic transformations of epigenetic marking and genome-wide transcriptional regulation that establish T cell identity [ChIP-Seq] GSE31234: Dynamic transformations of epigenetic marking and genome-wide transcriptional regulation that establish T cell identity [RNA-Seq] Refer to individual Series
2012-04-13 | E-GEOD-31235 | biostudies-arrayexpress
Project description:Dynamic Transformations of Genome-wide Epigenetic Marking and Transcriptional Control Establish T Cell Identity [RNA-Seq]
2015-04-13 | E-GEOD-31234 | ExpressionAtlas
Project description:Dynamic Transformations of Genome-wide Epigenetic Marking and Transcriptional Control Establish T Cell Identity [ChIP-Seq]
| PRJNA154107 | ENA
Project description:Dynamic Transformations of Genome-wide Epigenetic Marking and Transcriptional Control Establish T Cell Identity [RNA-Seq]
| PRJNA154109 | ENA
Project description:Pluripotency can be maintained in the naïve state through manipulation of ERK and WNT signalling (2i), shielding embryonic stem cells (ESCs) from inductive cues. Alternatively, inhibiting CDK8/19 (CDK8/19i), a repressor of the Mediator co-activator complex, directly stimulates super-enhancer activity, and was recently shown to stabilize cells in a functional state that resembles naïve pluripotency. Naïve ESCs exhibit important epigenetic, transcriptional and metabolic features. However, our understanding on how these regulatory layers are inter-connected to promote the naive state is in progress. To fill this gap, here we used mass spectrometry to describe the dynamic molecular events (i.e. phosphoproteome, proteome and metabolome) executed by 2i and CDK8/19i, as they transition cell identity into naïve pluripotency. We observed rapid proteomic reprogramming, revealing widespread commonalities, and some important differences, between these two approaches, suggesting a largely over-lapping mechanism. CDK8/19i acts directly on the control of the transcriptional machinery, which elicits a rapid and direct activation of key identity genes including those that maintain the naïve program. Additional molecular changes in 2i are achieved by phosphorylation of critical downstream effectors that reinforce the naïve transcriptional circuitry while repressing factors from the more-differentiated formative and primed states. Comparing transcriptomic and proteomic changes, we found that post-transcriptional de-repression is a major feature of naïve pluripotency conferred by both 2i and CDK8/19i, and this may support the enhanced mitochondrial capacity of naive cells. Furthermore, at the level of metabolome, while 2i- and CDK8/19i-treated cells share similar aspects in one-carbon metabolism and beta-oxidation, in other regards they are divergent, a feature which may explain their differences in DNA methylation. These datasets provide a valuable resource for exploring the molecular mechanisms underlying pluripotency and cell identity transitions.
2021-02-10 | PXD018694 | Pride
Project description:The balance between self-renewal and differentiation of hematopoietic stem cells (HSCs) is orchestrated by the combinatorial function of transcription factors and epigenetic regulators. Here, we report that the H4K16 acetyl-transferase MOF regulates chromatin accessibility and hematopoietic gene expression during erythroid commitment. Mof expression is controlled via a transcriptional feedforward pathway involving Runx1 and Gfi1b, which is crucial for the erythroid lineage bias. Single-cell RNA-seq of HSCs revealed that Mof haploinsufficient mice accumulate an otherwise rare HSC subset, indicating impaired differentiation.We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation.
2020-03-13 | GSE118194 | GEO
Project description:The balance between self-renewal and differentiation of hematopoietic stem cells (HSCs) is orchestrated by the combinatorial function of transcription factors and epigenetic regulators. Here, we report that the H4K16 acetyl-transferase MOF regulates chromatin accessibility and hematopoietic gene expression during erythroid commitment. Mof expression is controlled via a transcriptional feedforward pathway involving Runx1 and Gfi1b, which is crucial for the erythroid lineage bias. Single-cell RNA-seq of HSCs revealed that Mof haploinsufficient mice accumulate an otherwise rare HSC subset, indicating impaired differentiation.We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation.
2020-03-13 | GSE118192 | GEO
Project description:Cellular identity is ultimately dictated by the interaction of transcription factors with regulatory elements (REs) to control gene expression. Advances in genome-wide epigenome profiling techniques have significantly increased our understanding of cell-specific utilization of REs. However, it remains difficult to dissect the majority of factors that interact with these REs due to the lack of appropriate techniques. To address this issue, we developed a novel epigenetic method termed TINC: TALE-mediated Isolation of Nuclear Chromatin. Using TINC we interrogated the protein complex formed at the Nanog promoter in embryonic stem cells (ESCs) and identified many known interactors as well as numerous previously unknown complex members, including RCOR2. Further interrogation of the role of RCOR2 in the ESC network revealed its involvement in the repression of lineage genes and the fine-tuning of pluripotency genes. Consequently, using the Nanog promoter as a paradigm, we demonstrated the power of TINC to provide important insights into the molecular makeup of transcriptional complexes at individual REs as well as into control of cellular identity in general.
2020-12-14 | PXD022088 | Pride
Project description:The genetic programs that maintain leukemia stem cell (LSC) self-renewal and oncogenic potential have been well defined, however the epigenetic landscape that determines their cellular identity and functionality has not been established. We report that LSCs in MLL-associated leukemia are maintained in an epigenetic state defined by relative genome-wide high-level H3K4me3 methylation and low level H3K79me2. LSC differentiation is associated with dynamic reversal of these broad epigenetic profiles and concomitant down-regulation of the LSC maintenance transcriptional program. LSCs also share with embryonic stem cells a large subset of genes with bivalent histone marks related to embryonic development. The histone demethylase KDM5B negatively regulates MLL-induced leukemogenesis demonstrating the crucial role of the H3K4 global methylome for determining leukemia stem cell fate. Investigation of multiple histone modification marks and RNA Pol II in ckit+ and ckit- cells isolated and fractionated from MLL leukemia mice.
2015-06-26 | E-GEOD-60193 | biostudies-arrayexpress
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