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Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast [MeDIP-Seq]

ABSTRACT: Reprogramming of ES cells towards the trophoblast lineage, and specifally into self-renewing TS cells, can seemingly be achieved by manipulation of transcription factors such as Cdx2 and Oct4, or modulation of signalling cascades, notably Ras signalling. Here we analyze the arising cells from such treatment in detail for the efficiency and completeness of the reprogramming process. We find that the reprogrammed cells retain an epigenetic and transcriptional memory of their ES cell origin and are not equal to bona fide trophectoderm-derived TS cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE62138 | GEO | 2014/11/24

SECONDARY ACCESSION(S): PRJNA263268

REPOSITORIES: GEO

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Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast [RNA-Seq]

Project description:Reprogramming of ES cells towards the trophoblast lineage, and specifally into self-renewing TS cells, can seemingly be achieved by manipulation of transcription factors such as Cdx2 and Oct4, or modulation of signalling cascades, notably Ras signalling. Here we analyze the arising cells from such treatment in detail for the efficiency and completeness of the reprogramming process. We find that the reprogrammed cells retain an epigenetic and transcriptional memory of their ES cell origin and are not equal to bona fide trophectoderm-derived TS cells. RNA-seq expression analysis in conventional ES and TS cells and various ES-to-TS reprogramming models

2014-11-24 | E-GEOD-62149 | biostudies-arrayexpress

Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast [MeDIP-Seq]

Project description:Reprogramming of ES cells towards the trophoblast lineage, and specifally into self-renewing TS cells, can seemingly be achieved by manipulation of transcription factors such as Cdx2 and Oct4, or modulation of signalling cascades, notably Ras signalling. Here we analyze the arising cells from such treatment in detail for the efficiency and completeness of the reprogramming process. We find that the reprogrammed cells retain an epigenetic and transcriptional memory of their ES cell origin and are not equal to bona fide trophectoderm-derived TS cells. DNA methylation analysis in conventional ES and TS cells and various ES-to-TS reprogramming models

2014-11-24 | E-GEOD-62138 | biostudies-arrayexpress

Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast [RNA-Seq]

2014-11-24 | GSE62149 | 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

Mechanisms of transcription factor-mediated direct reprogramming of mouse embryonic stem cells to trophoblast stem-like cells

Project description:Direct reprogramming can be achieved by forced expression of transcription factors (TFs). Yet how such TFs mediate repression of initial cell-type-specific genes while activating target cell-type-specific genes is unclear. Here, we achieve embryonic stem (ES) to trophoblast stem (TS)-like cell reprogramming by introducing individual TS-specific “CAG” factors (Cdx2, Arid3a, Gata3). We interrogated their chromosomal target occupancies, modulation of global transcriptome and chromatin accessibility at the initial stage of reprograming. Our findings uncovered a sequential, two-step mechanism of cellular reprogramming in which repression of exiting ES pluripotency is followed by activated conversion to TS cells by CAG factors.

2017-07-25 | GSE90752 | GEO

Transcriptional Networks in Mouse Trophoblast Stem Cell Self-Renewal

Project description:Trophoblast stem cells (TS cells), derived from the trophectoderm (TE) of blastocysts, require transcription factors (TFs) and external signals (Fgf4, Activin/Nodal/Tgfb) for self-renewal. While many reports have focused on TF networks that regulate embryonic stem cell (ES cell) self-renewal and pluripotency, little is know about TF networks that regulate self-renewal in TS cells. To further understand transcriptional networks in TS cells we used chromatin immunopreciptiation and DNA microarray analysis (ChIP-chip) to investigate targets of TFs Ap-2g (Tcfap2c), Eomes, Ets2, and Gata3, and a chromatin remodeling factor, Brg1 (Smarca4). We then evaluated the transcriptional states of target genes using transcriptome analysis and genome-wide analysis of histone H3 acetylation (AcH3). Our results describe previously unknown transcriptional networks in TS cells, including TF occupancy of genes involved in ES cell self-renewal and pluripotency, co-occupancy of multiple TFs at target genes, and transcriptional regulatory circuitry within the 5 factors. Through genome-wide mapping and global expression analysis of 5 TF target genes, our data provide a comprehensive analysis of transcriptional networks that regulate TS cell self-renewal.

2010-02-09 | GSE18507 | GEO

Expression profiles in the complete absence of DNA methylation [Agilent-014868]

Project description:Using all three CpG DNA methyltransferases, Dnmt1, Dnmt3a and Dnmt3b deficient (TKO) mouse ES cells and TKO ntTS cells, we examined three histone modifications H3K4me2, H3K27me3 and H3K9me2, of promoter region in ES, TS and Flk1+ mesodermal cells with WT or TKO background by ChIP-chip analysis. Global profile analysis of gene expression and histone modification showed that the difference of profiles was mainly lineage dependent. Although the effects of DNA methylation loss in three lineages were modest, H3K27me3 is most sensitive to DNA methylation among three modifications. Interestingly, differentially expressed genes between WT and TKO cells were also lineage dependent and small number of genes was overlapped between lineages. Our further analysis showed that the profiles of H3K27me3 modifications were dynamically changed between lineages, especially in TS cells, and the pattern of H3K27me3 modification was defectively established by loss of DNA methylation. Our data suggest that DNA methylation contributes to lineage dependent expression regulation by collaborating with histone modification.

2021-02-17 | GSE36662 | GEO

Expression profiles in the complete absence of DNA methylation [Agilent-028005]

2021-02-17 | GSE36663 | GEO

Metabolic enhancement of developmental pausing (TS cells)

Project description:Embryonic stem (ES) cells and embryos reversibly pause via chemical mTOR inhibition. In this study, we investigate the tissue-specific response to mTORi-induced pausing in ES and trophoblast stem (TS) cells. To resolve the sequential rewiring of the proteome, we conducted a time-series proteomics experiment at 1, 3, 6, 12, 24, and 48 hours upon induction of pausing, and at 1, 3, 6, 12, 24, and 48 hours upon release of pausing in ES and TS cells. We find that ES, but not TS cells pause reversibly. To optimise developmental pausing conditions, we reasoned that by understanding the difference in pausing response of ES and TS cells, we could identify which pathways are essential for pausing. We found that KEGG pathways related to amino acid degradation, fatty acid degradation, and DNA repair are upregulated in ES cells, but downregulated in TS cells during entry into pausing. Moreover, by targeted metabolomics, we found a depletion of short chain carnitines in the paused ES cells. To extend the length of developmental pausing, we supplemented paused embryos with L-carnitine. The L-carnitine supplementation facilitates lipid usage and prolongs the pausing length by 19 days through the establishment of a more dormant state.

2023-11-06 | PXD033798 | Pride

Metabolic enhancement of developmental pausing (ES dataset)

2023-11-06 | PXD033750 | Pride

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