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Modulation of HDAC activity directly reprogramme embryonic stem cell to trophoblast stem cell [ChIP-Seq]

ABSTRACT: Modulation of HDAC activity directly reprogramme embryonic stem cell to trophoblast stem cell [ChIP-Seq]

PROVIDER: PRJNA794742 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17446842_1.fastq.gz	Fastqsanger.gz
	SRR17446842_2.fastq.gz	Fastqsanger.gz
	SRR17446843_1.fastq.gz	Fastqsanger.gz
	SRR17446843_2.fastq.gz	Fastqsanger.gz
	SRR17446844_1.fastq.gz	Fastqsanger.gz

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Modulation of HDAC activity directly reprogramme embryonic stem cell to trophoblast stem cell

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Modulation of HDAC activity directly reprogramme embryonic stem cell to trophoblast stem cell [bulk RNA-Seq]

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Modulation of HDAC activity directly reprogramme embryonic stem cell to trophoblast stem cell [ChIP-Seq]

Project description:Embryonic stem cells (ESCs) can differentiate into all cell types of each of the embryonic germ layers. ESCs can also generate totipotent 2C-like cells and trophectodermal cells. However, these latter transitions occur at low frequency due to epigenetic barriers, the nature of which are not fully understood. Here, we show that mouse ESCs treated with sodium butyrate, an HDAC inhibitor, have a greatly increased 2C-like cell population and can transdifferentiate into trophoblast stem cells (TSCs). Interestingly, this ESC to TSC transition is a direct reprogramming event that does not require transition through a 2C-like state. Mechanistically, butyrate inhibits Class I histone deacetylases activities in LSD1-HDAC1/2 corepressor complex, increasing acetylation levels in the regulatory regions of 2C and TSC specific genes. Importantly, butyrate treated cells acquire the capacity to generate blastocyst-like structures that can develop beyond the implantation stage in vitro and induce decidualization in vivo. These results uncover how epigenetic changes can expand the potency of ESCs.

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Inhibition of HDAC activity directly reprograms murine embryonic stem cells to trophoblast stem cells

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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.

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Modulation of HDAC activity directly reprogramme embryonic stem cell to trophoblast stem cell

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

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