GEO accession GSE209718 is currently private and is scheduled to be released on Dec 31, 2025.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA862143 | ENA |
REPOSITORIES: ENA
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Project description:FGF signaling is thought to be important for linegae specification during mouse develoipment. However, we have recently observed that FGF4 and FGF2 have opposing effects on Erk activity and ultimately on cell fate in both mouse embryonic stem cells and embryos. The aim of this study was to understand, at a single cell level, the impact in lineage specification of early exposure to FGF2 or FGF4 in gastruloid formation, a new 3D in vitro model of mouse gastrulation.
2025-12-31 | GSE209718 | GEO
Project description:FGF2 and FGF4 treatment of mouse embryonic stem cells (mESC) was shown to induce different levels of Nanog expression in mES cells and gastruloids and consequently, give rise to differences in lineage specification during early gastrulation. The aim of this study was to identify genes regulated by Nanog that underlie these biases in lineage specification
2025-12-31 | GSE209717 | GEO
Project description:Nanog expression at naïve to prime transition biases lineage specification [CHIP-seq]
| PRJNA862144 | ENA
Project description:It is well documented that differentiation of stem cells is generally associated with and facilitated by an elongated cell cycle. However, for lineage specification requiring high ERK activity, which also promotes proliferation, it is unclear how stem cells simultaneously negotiate the “proliferation-differentiation” decision. Here we investigate this question using multiplex quantitative live-cell imaging to track embryonic stem cells (ESC) differentiation into mesendoderm (ME) lineage with high ERK activity. We show that ERK activity increase manifested by a heightened ERK oscillation frequency drove robust ME differentiation accompanied by a modest cell cycle acceleration. We profile the responses of ME differentiation and cell cycle length as a function of a synthetic ERK oscillatory activity gradient. Our results reveal that these two processes took place in distinct ranges of ERK oscillation frequency, with ME differentiation requiring higher level for ERK oscillation to secure efficient ME protein translation. Interactions between gastrulation morphogens recapitulated an ERK oscillation gradient, potentiating heterogeneous ME fates while maintaining a comparable level of proliferation. Our study thus provides mechanistic insights into how ERK fine-tunes proliferation and differentiation during cell fate specification
2026-02-23 | GSE273286 | GEO
Project description:In mammals, primordial germ cells (PGCs), the origin of the germ line, are specified from the epiblast at the posterior region where gastrulation simultaneously occurs, yet the functional relationship between PGC specification and gastrulation remains unclear. Here, we show that Ovol2, a transcription factor conserved across the animal kingdom, balances these major developmental processes by repressing the epithelial-to-mesenchymal transition (EMT) driving gastrulation and the upregulation of genes associated with PGC specification. Ovol2a, a splice variant encoding a repressor domain, directly regulates EMT-related genes and consequently induces re-acquisition of potential pluripotency during PGC specification, whereas Ovol2b, another splice variant missing the repressor domain, directly upregulates genes associated with PGC specification. Taken together, these results elucidate the molecular mechanism underlying allocation of the germ line among epiblast cells differentiating into somatic cells through gastrulation.
2022-01-26 | GSE184650 | GEO
Project description:In mammals, primordial germ cells (PGCs), the origin of the germ line, are specified from the epiblast at the posterior region where gastrulation simultaneously occurs, yet the functional relationship between PGC specification and gastrulation remains unclear. Here, we show that Ovol2, a transcription factor conserved across the animal kingdom, balances these major developmental processes by repressing the epithelial-to-mesenchymal transition (EMT) driving gastrulation and the upregulation of genes associated with PGC specification. Ovol2a, a splice variant encoding a repressor domain, directly regulates EMT-related genes and consequently induces re-acquisition of potential pluripotency during PGC specification, whereas Ovol2b, another splice variant missing the repressor domain, directly upregulates genes associated with PGC specification. Taken together, these results elucidate the molecular mechanism underlying allocation of the germ line among epiblast cells differentiating into somatic cells through gastrulation.
2022-01-26 | GSE184644 | GEO
Project description:Endogenously generated sulfides are conserved among species and tissues and exert multiple effects through diverse mechanisms. Although sulfides have been linked to cell fates, their role in pluripotent stem cell commitment remains unknown. Here we discovered that during directed differentiation of induced pluripotent stem cells, endogenous sulfide levels drop in all three germ layers, with the mesodermal lineage exhibiting the lowest capacity to generate these species at early specification events. Addition of a rapid releasing sulfide donor in iPSCs or mesodermal cells did not affect the redox surveillance mechanisms, however altered persulfidation and transcription of cell fate commitment pathways. In particular, sulfide supplementation in pluripotent stem cells reduced cell differentiation processes by preserving the activity of the stem cell transcription factors OCT4 and KLF4. In contrast, supplementation of sulfide during mesodermal lineage specification promoted persulfidation and activated the WNT signaling as well as enriched the activity of the ETS transcription factor family, resulting in increased transcription of angiogenic and vessel morphogenesis genes. Sulfide addition during the development of vascular organoids enhanced blood vessel morphogenesis. Taken together, these data position protein persulfidation as a timing-dependent regulator that preserves pluripotency prior to commitment but subsequently biases mesoderm toward endothelial specification, thereby emerging as a tractable redox modification for engineering stem cell fate and vascularization.
2025-12-29 | PXD071015 | Pride
Project description:Fgf signaling via Erk activation has been associated with both neural induction and the generation of a primed state for the differentiation of embryonic stem cells (ESCs) to all somatic lineages. To dissect the role of Erk in both ESC self-renewal and lineage specification we explore the requirements for this pathway in various in vitro differentiation settings. A combination of pharmacological inhibition of Erk signaling and genetic loss of function experiments reveal a role for Erk signaling in suppressing endodermal differentiation, but not neural specification. Activation of Erk signaling in ESCs de-represses primitive endoderm (PrE) gene expression as a consequence of inhibiting the pluripotent/epiblast network. The early response to Erk activation correlates with functional PrE priming while sustained Erk activity results in PrE differentiation. Taken together, our results suggest that Erk signaling suppresses pluripotent gene expression to enable endodermal differentiation. We use microarray analysis to determine the transcription response to Erk1/2 in mouse embryonic stem cells across a 24 hour window of time Mouse ESCs carrying a tamoxifen inducible constitutively active c-Raf fusion protein were stimulated for 6 time points (30minutes, 1 hour, 2 hours, 4 hours, 8 hours, and 24 hours) in the presence of 250nM PD173074. Uninduced (0h hours) and DMSO only treated cells served as controls.
2015-01-01 | E-GEOD-59755 | biostudies-arrayexpress
Project description:The amnion, an essential extra-embryonic tissue in mammalian embryos, is thought to provide crucial signaling, structural and nutritional support during pregnancy. Despite its pivotal importance, studying primate amnion formation and function has been hampered by the lack of accurate in-vitro models. Here, we present a human embryonic stem cell-derived 3D model of the post-gastrulation amnion (PGA) that faithfully recapitulates extra-embryonic development up to 4-weeks post-fertilization closely mimicking the functional traits of the human amniotic sac. PGAs self-organize forming the amnion and the yolk sac and are surrounded by extra-embryonic mesoderm, which forms a connecting stalk. Using PGAs, we show that GATA3 is required and sufficient for amniogenesis and reveal an autoregulatory feedback loop governing amnion formation, whereby extra-embryonic signals promote amnion specification. The reproducibility and scalability of the PGA system, with its precise cellular composition and structural integrity, opens new avenues for investigating embryo-amnion interactions beyond gastrulation and offers an ideal platform for large-scalegenetic, pharmacological, and biomechanical studies.
2026-01-19 | PXD062917 | Pride
Project description:The gastrulation process is controlled by the interplay between morphogenetic signals from BMP, WNT and NODAL pathways. Increasing evidences support an emerging role of the Hippo-YAP signaling in the cell-fate decisions that guide lineage specification in mouse and human Embryonic Stem Cells (hESCs). However, the contribution of YAP to the process of gastrulation in hESCs remains unknown. Here, we show that YAP1 regulates the specification, size and patterning of the three-germ layers. Using hESC-derived 2D-micropatterned gastruloids and directed differentiation approaches we show that YAP maintains a semi-active NODAL signaling during gastrulation essential to regulate the exit of pluripotency. In absence of YAP1, a hyperactive NODAL signaling retains SMAD2.3 in the nuclei, impeding the exit of pluripotency and the acquisition of the ectodermal gene program. Accordingly, the inhibition of NODAL signaling is sufficient to rescue the gastrulation-defective phenotype of the YAP1 KO hESCs. Our work revealed that Hippo-YAP1 signaling is an important component of the developmental network that coordinate hESC pluripotency and gastrulation.
2022-01-14 | GSE168377 | GEO