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RNAseq and ChIPseq on Mouse Embryonic Stem Cells and Sorted Mesendoderm Progenitor Cells [ChIP-seq]

ABSTRACT: We mapped the enhancer and long non-coding transcriptional landscape during mesendoderm specification. Mesendodermal progenitors were sorted from differentiating ESCs according to Eomes expression. Enhancer usage was coordinated with mesendoderm-specific expression of key lineage-determining transcription factors. We demonstrated that many of these enhancers are associated with the expression of lncRNAs.

ORGANISM(S): Mus musculus

PROVIDER: GSE103262 | GEO | 2017/10/10

SECONDARY ACCESSION(S): PRJNA401912

REPOSITORIES: GEO

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RNAseq and ChIPseq on Mouse Embryonic Stem Cells and Sorted Mesendoderm Progenitor Cells [RNA-seq]

Project description:We mapped the enhancer and long non-coding transcriptional landscape during mesendoderm specification. Mesendodermal progenitors were sorted from differentiating ESCs according to Eomes expression. Enhancer usage was coordinated with mesendoderm-specific expression of key lineage-determining transcription factors. We demonstrated that many of these enhancers are associated with the expression of lncRNAs.

2017-10-10 | GSE103261 | GEO

Changing the Waddington landscape to control mesendoderm competence -- ATAC-seq

Project description:As pluripotent human embryonic stem cells progress towards one germ layer fate, they lose the ability to adopt alternative fates. It is unknown how the cells’ competence for these alternative fates changes along their developmental trajectory or if this competence can be modulated. Here, we show that a differentiating stem cell’s probability of adopting a mesendodermal fate when given the appropriate signal falls sharply at a specific point along the ectodermal trajectory, and we further demonstrate that this point can be moved using genetic perturbations. Using a low-dimensional reaction coordinate to monitor progression towards ectoderm, we can determine the probability that individual cells at different points along this path can transition to the mesendodermal fate upon BMP4 and Activin A signal exposure. Knowing this probability allows us to prospectively isolate and profile differentiating cells based on their mesendoderm competence. Analysis and validation of these RNA-seq and ATAC-seq profiles identified transcription factors that can independently control the cell’s mesendoderm competence and its progression along the ectodermal developmental trajectory. In the classical picture of a Waddington landscape, these effects correspond to altering the barrier between fates and changing the cell’s location on the landscape, respectively. The ability of the underlying gene regulatory network to modulate these two aspects of the developmental landscape could allow separate control of the dynamics of differentiation and tissue size proportions.

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2009-06-12 | E-MEXP-1672 | biostudies-arrayexpress

Whsc1 controls mesendodermal transcription factor expression

Project description:We report here chromatin related factor Whsc1 links pluripotency exit and mesendodermal differentiation. We performed RNA-seqs to compare Whsc1+/+ and Whsc1-/- embryonic stem cells (ESCs) to compare the transcriptomes. UMI-4C experiments have been performed to identify regions having contacts with promoter regions of downstream Whsc1 targets: the mesendoderm transcritpion factors

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RNAseq and ChIPseq on Mouse Embryonic Stem Cells and Sorted Mesendoderm Progenitor Cells

Project description:RNAseq and ChIPseq on Mouse Embryonic Stem Cells and Sorted Mesendoderm Progenitor Cells

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ChIP-seq of FOXK2 in human embryonic stem cells H1 ESC, and the differentiated mesendoderm cells and and NPC cells

Project description:In order to investigate the genome-wide binding profile of the forkhead transcription factor FOXK2 in human embryonic stem cells (ESCs) and downstream cell types, we generated the ChIP-seq data of FOXK2 in H1 ESC cells and two differentiated types of cells, mesendoderm cells and NPC cells.

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p53 coordinates Wnt and TGF-β inputs on mesendoderm differentiation genes

Project description:The TGF-β superfamily member Nodal triggers mesendoderm differentiation in embryonic stem (ES) cells. This transition however requires cooperating Wnt signaling inputs. Here we report that p53, a powerful tumor suppressor in adult tissues, orchestrates this cooperation. We show that p53, which is released from inhibition as mouse ES cells exit from pluripotency, acts as a direct inducer of Wnt3 expression. Wnt-activated Tcf3 then converges with Nodal-activated Smad transcriptional complexes on mesendoderm specification super-enhancers. p53 and its homolog p73 act redundantly in Wnt induction. When p53 and p73 are depleted, the ES cells fail to secrete autocrine Wnt ligands, Tcf and Nodal-activated Smads fail to bind to mesendoderm gene enhancers, and the cells adopt ectoderm rather than mesendoderm identity. Enforced Wnt3 expression or addition of Wnt3a rescues mesendoderm differentiation in p53/p73-depleted ES cells. Thus, independently of their established role as tumor suppressors that guard genome integrity in mature cells, p53 and p73 serve a primordial role in ES cell differentiation by driving a cooperation of Wnt and TGF-β transcriptional inputs on mesendoderm identity gene enhancers.

2017-01-06 | GSE70486 | GEO

RNAseq and ChIPseq on Mouse Embryonic Stem Cells and Sorted Mesendoderm Progenitor Cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-10-10 | GSE103263 | GEO

HUES cells: control and overexpressing OCT4

Project description:HUES24 cell line was nucleofected with POU5f1 cDNA to overexpress OCT4; This leads to the formation of mesendodermal cells Short- and Long-scales intra- and inter-chromosomal interactions are linked to gene transcription, but the molecular event underlying these structures and how it affects cell fate decision during embryonic development are poorly understood. One of the first embryonic cell fate decisions (i.e mesendoderm determination) is driven by the POU factor OCT4, acting in concert with the high mobility group genes SOX-2 and SOX-17. Here, we identify novel chromatin remodelling mechanism and enhancer function driven by both OCT4 and SALL4 that mediate cell fate switching. We found that OCT4 alters the higher-order chromatin structure at both Sox-2 and Sox-17 loci. OCT4 titrates out cohesin and switches the Sox-17 enhancer from a locked (within an inter-chromosomal Sox-2 enhancer/CTCF/cohesin loop) to an active (within an intra-chromosomal Sox-17 promoter/enhancer/cohesin loop) state. SALL4 concomitantly mobilizes the polycomb complexes at the Soxs loci. Thus, OCT4/SALL4-driven cohesin-and polycombs-mediated changes in higher order chromatin structure mediate instruction of early cell fate in embryonic cells. ChIP anti-OCT4 on chip. results_v2.xls file description: Enriched binding sites. Mutant means oct4 overexpressing cells , wt GFP nucleofected cells.

2015-04-02 | E-GEOD-58125 | biostudies-arrayexpress

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