Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA313518 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3196373_1.fastq.gz | Fastqsanger.gz | |||
| SRR3196373_2.fastq.gz | Fastqsanger.gz | |||
| SRR3196374_1.fastq.gz | Fastqsanger.gz | |||
| SRR3196374_2.fastq.gz | Fastqsanger.gz | |||
| SRR3196375_1.fastq.gz | Fastqsanger.gz |
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Project description:Here we report a potent, acetyl-lysine competitive and cell active inhibitor, PFI-3, that tightly binds to the bromodomain present in BRG1/BRM and the fifth bromodomain in Polybromo (BAF180). The high specificity of PFI-3 was achieved based on a novel binding mode of a salicylic acid head group that led to the replacement of water molecules typically maintained in bromodomain inhibitor complexes. Embryonic stem cells exposure to PFI-3 led to deprivation of stemness and deregulated lineage specification. Furthermore, differentiation of trophoblast stem cells in the presence of PFI-3 was dramatically enhanced. TSC were treated with PF1-3 or control compound in stemness or differentiation conditions, 2 replicates were used for treatment in stemness and differentiation conditions together with 2 control replicates in stemness and one during differentiation; DFKZ genomics and proteomics
2015-12-16 | E-GEOD-65358 | biostudies-arrayexpress
Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation. Mouse trophoblast stem cells (TSCs) were isoloated from a single conditional Lsd1-deficient mouse (Lsd1tm1SchM-CM-<le). Deletion of Lsd1 was induced eight days before the collection of RNA by addition of 0.2 M-BM-5M 4OH-tamoxife. Cells were isolated at successive stages of differentiation for total RNA extraction and hybridization on Affymetrix microarrays. To that end, we harvested cells at three time-points: before induction of differentiation (d0), two days after induction of differentiation (d2), and four days after induction of differentiation (d4). Three replicates (1, 2, 3) for control (-) and Lsd1-deficeint (+) cells were included for each differentiation stage.
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Project description:Trophoblast stem cells (TSC) global transcriptome in stemness and differentiation conditions after treatment with PF1-3
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Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation.
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Project description:We derive experimental conditions for the derivation of marmoset trophoblast like cells. Marmoset naïve PSC form extraembryonic mesoderm in human TSC conditions, whilst TGFβ/NODAL, FGF/ERK and WNT signalling control marmoset peri- and postimplantation trophoblast identity.
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2015-12-01 | PXD003145 | Pride
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.
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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.
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