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ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2 [ChIP-seq]

ABSTRACT: ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2 [ChIP-seq]

PROVIDER: PRJNA746346 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15128352_1.fastq.gz	Fastqsanger.gz
	SRR15128352_2.fastq.gz	Fastqsanger.gz
	SRR15128353_1.fastq.gz	Fastqsanger.gz
	SRR15128353_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

ESRRB Facilitates the Conversion of Trophoblast-like Stem Cells from Induced Pluripotent Stem cells by Directly Regulating KRT8 and CDX2

Project description:Porcine induced pluripotent stem cells (piPSCs) could serve as a great model system for human stem cell pre-clinical research. However, the pluripotency gene network of piPSCs, especially the function for the core transcription factor ESRRB, was poorly understood. Here, we constructed ESRRB-overexpressing piPSCs (ESRRB-piPSCs). Compared with the control piPSCs (CON-piPSCs), the ESRRB-piPSCs showed flat, monolayered colony morphology. Moreover, the ESRRB-piPSCs showed greater chimeric capacity into trophectoderm than CON-piPSCs. We found that ESRRB could directly regulate the expressions of trophoblast stem cell (TSC)-specific markers, including KRT8, KRT18 and CDX2, through binding to their promoter regions. Mutational analysis proved that the N-terminus zinc finger domain is indispensable for ESRRB to regulate the TSC markers. Furthermore, this regulation needs the participation of OCT4. Accordingly, the cooperation between ESRRB and OCT4 facilitates the conversion from pluripotent state to the trophoblast-like state.

2022-02-17 | PXD027539 | Pride

ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2 [RNA-seq]

Project description:Studies on porcine induced pluripotent stem cells (piPSCs) served as a great reference for human clinical research. However, the pluripotency genes network of piPSCs, especially the core transcription factor ESRRB, was currently poor understand. Here, we constructed an overexpressing ESRRB piPSC line (ESRRB piPSCs) in which ESRRB expression was efficiently enhanced. It was found that ESRRB piPSCs showed scattered and flat colonies, moreover, the ESRRB piPSCs showed higher chimeric capacity into trophectoderm than that of CON piPSCs. We also found that ESRRB could directly regulate the expressions of the trophoblast stem cells (TSCs) markers, such as KRT8, KRT18 and CDX2, through binding in their promoter regions. Functional analysis of the mutant domains of ESRRB proved. that the zinc finger domain was indispensable for ESRRB to regulate TSCs markers. Moreover, the regulated process needed the participation of OCT4. Accordingly, ESRRB cooperating with OCT4 promoted TSCs markers to facilitate the conversion from the pluripotent state to trophoblastic-like state. Our results revealed the unique and crucial role of ESRRB in the determination of piPSCs fate and provided opportunities for studying the barriers underlying embryonic and extra-embryonic lineage segregation.

2021-10-14 | GSE180057 | GEO

ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2 [ChIP-seq]

2021-10-14 | GSE180056 | GEO

ESRRB Facilitates the Conversion of Trophoblast-Like Stem Cells From Induced Pluripotent Stem Cells by Directly Regulating CDX2.

Project description:Porcine-induced pluripotent stem cells (piPSCs) could serve as a great model system for human stem cell preclinical research. However, the pluripotency gene network of piPSCs, especially the function for the core transcription factor estrogen-related receptor beta (ESRRB), was poorly understood. Here, we constructed ESRRB-overexpressing piPSCs (ESRRB-piPSCs). Compared with the control piPSCs (CON-piPSCs), the ESRRB-piPSCs showed flat, monolayered colony morphology. Moreover, the ESRRB-piPSCs showed greater chimeric capacity into trophectoderm than CON-piPSCs. We found that ESRRB could directly regulate the expressions of trophoblast stem cell (TSC)-specific markers, including KRT8, KRT18 and CDX2, through binding to their promoter regions. Mutational analysis proved that the N-terminus zinc finger domain is indispensable for ESRRB to regulate the TSC markers. Furthermore, this regulation needs the participation of OCT4. Accordingly, the cooperation between ESRRB and OCT4 facilitates the conversion from pluripotent state to the trophoblast-like state. Our results demonstrated a unique and crucial role of ESRRB in determining piPSCs fate, and shed new light on the molecular mechanism underlying the segregation of embryonic and extra-embryonic lineages.

| S-EPMC8488167 | biostudies-literature

ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2

Project description:ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2

| PRJNA746345 | ENA

ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2 [RNA-seq]

Project description:ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2 [RNA-seq]

| PRJNA746347 | ENA

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

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [ChIP-Seq]

Project description:Trophoblast stem cells (TSCs) are derived from the trophoectoderm of a blastocyst and can maintain self-renewal in vitro. Meanwhile, essential insights into the molecular mechanisms controlling placental developmental could be gained by using TSCs that can differentiate into the various placental trophoblast cell types in vitro. Esrrb is a transcription factor with pivotal roles in maintaining TSCs’ self-renewal, but the exact transcriptional networks that Esrrb involved in TSCs are largely unknown. In the present study, we elucidated the function of Esrrb during TSC self-renewal and differentiation. We demonstrate that precise levels of Essrb are critical for TSCs stemness maintenance and normal trophoblast differentiation, as Esrrb depletion results in down-regulation of the key TSC-specific transcription factors, consequently causing TSCs differentiation and forced expression of Esrrb can partially block TSCs differentiation in the absence of FGF4. This function of Esrrb is exerted by directly binding and activating a core set of TSC-specific target genes including Cdx2, Eomes, Sox2, Fgfr4 and BMP4. Furthermore, we investigate the role of Esrrb in reprogramming of mouse embryonic fibroblasts (MEFs) to induced TSCs (iTSCs). We show that Esrrb can facilitate the conversion of iTSCs from MEFs. Moreover, Esrrb can substitute for Eomes during this conversion process. Our findings provide a better understanding of the molecular mechanism of Esrrb in maintaining TSCs self-renewal and iTSCs reprogramming.

2019-10-06 | GSE104695 | GEO

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [RNA-Seq]

2019-10-06 | GSE104694 | GEO

Dynamics of Sox2 and Esrrb occupancy during the differentiation of embryonic stem cells into trophoblast stem cells.

Project description:To understand the mechanism underlying the versatility in transcriptional regulation by Sox2 and Esrrb, we compared genome-wide binding sites of Sox2 and Esrrb in embryonic stem (ES) cells and trophoblast stem (TS) cells by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq).

2013-10-17 | GSE28453 | GEO

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