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Dosage-dependent role of Gata3 in primitive endoderm and trophectoderm specification in embryonic stem cells [scRNA-Seq]

ABSTRACT: Transcription factors (TFs) are critical regulators of cell fate decisions, and their intricate balance determines lineage specification during early development. Gata3 is a well-established TF in the trophectoderm (TE) development, and its ectopic expression can reprogram mouse embryonic stem (ES) cells into trophoblast stem (TS) cells. Because of Gata3’s canonical role in TE, its potential involvement in primitive endoderm (PE) differentiation has remained unexamined, representing a previously overlooked avenue of investigation. Here, we reveal that Gata3 functions as a dosage-sensitive switch governing lineage commitment in mouse ES cells. Modulating Gata3 expression revealed that high levels (Gata3-H) drive TE specification, whereas lower levels (Gata3-L) promote PE differentiation, as evidenced by distinct morphological transitions, transcriptional profiles, chromatin-binding, and functional assays. Mapping targets of Gata3 revealed differential occupancy patterns at PE- versus TE-associated enhancers correlating with dose. In vitro 3D blastoid models confirmed that Gata3 dosage alone is sufficient to drive spatial segregation, with Gata3-L and Gata3-H cells preferentially localizing to PE- and TE-like compartments, respectively. Our findings highlight Gata3’s pioneer factor-like behavior, downregulation of pluripotency networks, and latent capacity to direct lineage specification beyond its classical TE specification. These results expand the understanding of Gata family TFs in early embryogenesis and provide mechanistic insights for stem-cell based models for lineage specification.

ORGANISM(S): Mus musculus

PROVIDER: GSE327389 | GEO | 2026/07/06

REPOSITORIES: GEO

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Dosage-dependent role of Gata3 in primitive endoderm and trophectoderm specification in embryonic stem cells [ChIP-seq]

Project description:Transcription factors (TFs) are critical regulators of cell fate decisions, and their intricate balance determines lineage specification during early development. Gata3 is a well-established TF in the trophectoderm (TE) development, and its ectopic expression can reprogram mouse embryonic stem (ES) cells into trophoblast stem (TS) cells. Because of Gata3’s canonical role in TE, its potential involvement in primitive endoderm (PE) differentiation has remained unexamined, representing a previously overlooked avenue of investigation. Here, we reveal that Gata3 functions as a dosage-sensitive switch governing lineage commitment in mouse ES cells. Modulating Gata3 expression revealed that high levels (Gata3-H) drive TE specification, whereas lower levels (Gata3-L) promote PE differentiation, as evidenced by distinct morphological transitions, transcriptional profiles, chromatin-binding, and functional assays. Mapping targets of Gata3 revealed differential occupancy patterns at PE- versus TE-associated enhancers correlating with dose. In vitro 3D blastoid models confirmed that Gata3 dosage alone is sufficient to drive spatial segregation, with Gata3-L and Gata3-H cells preferentially localizing to PE- and TE-like compartments, respectively. Our findings highlight Gata3’s pioneer factor-like behavior, downregulation of pluripotency networks, and latent capacity to direct lineage specification beyond its classical TE specification. These results expand the understanding of Gata family TFs in early embryogenesis and provide mechanistic insights for stem-cell based models for lineage specification.

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Dosage-dependent role of Gata3 in primitive endoderm and trophectoderm specification in embryonic stem cells [RNA-seq]

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Fosl1 transdifferentiate embryonic stem cells to differentiated trophoblast stem cells (RNA-seq)

Project description:During mammalian embryonic development, the first lineage commitment event gives rise to two distinct cell populations: the trophectoderm (TE) and the inner cell mass (ICM). The TE consists of outer cells of the blastocyst and ultimately forms the placenta while the ICM gives rise to all the embryonic tissues. Numerous transcription factors (TFs) guiding ICM differentiation into different embryonic tissues have been characterized. However, only a few TFs that are required for TE specification and differentiation have been identified, and much less is understood as to how these TFs interact with other TFs or with their chromosomal targets in order to drive cell fate towards TE lineage. Understanding trophectoderm development is crucial because cells in this lineage are required for proper embryo implantation in the uterus. Defects in this lineage can cause early failure of pregnancy as well as other pregnancy related disorders such as preeclampsia and intrauterine growth restriction (IUGR). Here, we characterize the function of one of TE-specific TF, Fosl1, which was previously suggested as having some role in placental development. We utilized mouse embryonic stem (ES) cells (derived from ICM) and showed that ectopic expression of Fosl1 can transdifferentiate ES cells to differentiated TS cells (trophoblast giant-like cells). We show that Fosl1 does so by directly binding and activating TE specific genes and genes associated with epithelial-mesenchymal transition (EMT). Using mouse trophoblast stem (TS) cells, we also establish that Fosl1 is required for specification of TS cells to trophoblast giant cells (TGCs) subtype. Therefore, we postulate that Fosl1 is a key regulator of TS cell differentiation.

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Fosl1 transdifferentiate embryonic stem cells to differentiated trophoblast stem cells. (ChIP-seq)

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Functional role of GATA3 and CDX2 in lineage specification during bovine early embryonic development

Project description:Current understandings of the initiation of the trophectoderm (TE) program in mammalian embryonic development lacks evidence of how TE-associated factors such as CDX2 and GATA3 participate in bovine lineage specification. In this study, we describe the effects of TE-associated factors on lineage specification marker genes such as SOX2, OCT4, NANOG, GATA6 and SOX17, assisted by a cytosine base editor system. Interestingly, GATA3 downregulates the NANOG expression in bovine blastocysts. Further analysis of the blastocyst mosaic shows that GATA3 is required for NANOG in TE cells of bovine blastocysts. It is worthy to notice that, unlike mouse embryos where GATA3 and CDX2 did not reciprocally affect each other in bovine embryos.

2022-10-26 | GSE216123 | GEO

The TH1 cell lineage-determining transcription factor T-bet supresses TH2 gene expression by redistributing GATA3 away from TH2 genes [ChIP-seq]

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The TH1 cell lineage-determining transcription factor T-bet supresses TH2 gene expression by redistributing GATA3 away from TH2 genes [RNA-seq]

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Arid3a modulates the first cell fate decision by direct regulation of both embryonic and extraembryonic gene expression (ChIP-Seq)

Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a ChIP was performed using bioChIP-sequencing. Control ChIP-sequencing was performed using BirA cells. HDAC1 ChIP was performed as native antibody ChIP-sequencing.

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