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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [scRNA-Seq]

ABSTRACT: A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [scRNA-Seq]

PROVIDER: PRJNA856234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19997363_1.fastq.gz	Fastqsanger.gz
	SRR19997363_2.fastq.gz	Fastqsanger.gz

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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation

Project description:A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation

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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ATAC-Seq]

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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [RNA-Seq]

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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ChIP-Seq]

Project description:A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ChIP-Seq]

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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [scRNA-Seq]

Project description:Cooperative DNA binding of transcription factors (TFs) integrates external stimuli and context across tissues and time. Naïve mouse embryonic stem cells (ESCs) are derived from early development and can sustain early embryonic pluripotent identity indefinitely. Here we ask whether TFs associated with pluripotency evolved to directly support this state or if it emerges from their combinatorial action? NANOG and ESRRB are key pluripotency factors that co-bind DNA. We find that when both factors are expressed at physiological levels, ESRRB supports pluripotency. However, when NANOG is not present, ESRRB supports a bistable culture of embryo-like primitive endoderm identity ancillary to pluripotency. The stochiometry between these factors quantitatively influences differentiation and in silico modelling of bipartite TF activity suggests ESRRB safeguards plasticity in differentiation. Thus the concerted activity of cooperative TFs transforms their effect to sustain intermediate cell identities that can be expanded ex vivo as highly stable stem cell models.

2023-04-18 | GSE207564 | GEO

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ATAC-Seq]

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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ChIP-Seq]

2023-04-18 | GSE207562 | GEO

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [RNA-Seq]

2023-04-18 | GSE207560 | GEO

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation

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

2023-04-18 | GSE207565 | GEO

Fgf and Esrrb integrate epigenetic and transcriptional networks that regulate self-renewal of Trophoblast Stem Cells

Project description:Esrrb is a transcription factor implicated in embryonic stem (ES) cell self-renewal, yet its knockout causes intrauterine lethality due to defects in trophoblast development. Here we show that in trophoblast stem (TS) cells, Esrrb is a downstream target of fibroblast growth factor (Fgf) signalling and is critical to drive TS cell self-renewal. In contrast to its occupancy of pluripotency-associated loci in ES cells, Esrrb sustains the stemness of TS cells by direct binding and regulation of TS cell-specific transcription factors including Elf5 and Eomes. To elucidate the mechanisms whereby Esrrb controls the expression of its targets, we characterized its TS cell-specific interactome by mass spectrometry. Unlike in ES cells, Esrrb interacts in TS cells with the histone demethylase Lsd1 and with the RNA Polymerase II-associated Integrator complex. Our findings provide new insights into both, the general and context-dependent wiring of transcription factor networks in stem cells by master transcription factors.

2015-07-24 | PXD002183 | Pride

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