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VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification

ABSTRACT: VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification

PROVIDER: PRJNA796951 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17607102.fastq.gz	Fastqsanger.gz
	SRR17607103.fastq.gz	Fastqsanger.gz
	SRR17607104_1.fastq.gz	Fastqsanger.gz
	SRR17607104_2.fastq.gz	Fastqsanger.gz
	SRR17607105_1.fastq.gz	Fastqsanger.gz

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VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification [scRNA-Seq]

Project description:In contrast to rodents, the mechanisms underlying human trophectoderm and early placenta specification are understudied due to ethical barriers and the scarcity of embryos. Recent reports have shown that human pluripotent stem cells (PSCs) can differentiate into trophectoderm (TE)-like cells (TELCs) and trophoblast stem cells (TSCs), offering a valuable in vitro model to study early placenta specification. Here, we demonstrate that the VGLL1 (vestigial-likefamilymember1), which is highly expressed during human and non-human primate TE specification in vivo but is negligibly expressed in mouse, is a critical regulator of cell fate determination and self-renewal in human TELCs and TSCs derived from naïve PSCs. Mechanistically, VGLL1 partners with the transcription factor TEAD4 (TEA domain transcription factor 4) to regulate chromatin accessibility at target gene loci through histone acetylation and acts in cooperation with GATA3 and TFAP2C. Our work is relevant to understand primate early embryogenesis and how it differs from other mammalian species.

2024-01-05 | GSE252377 | GEO

VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification [scRNA-Seq]

Project description:VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification [scRNA-Seq]

| PRJNA1060312 | ENA

VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification.

Project description:In contrast to rodents, the mechanisms underlying human trophectoderm and early placenta specification are understudied due to ethical barriers and the scarcity of embryos. Recent reports have shown that human pluripotent stem cells (PSCs) can differentiate into trophectoderm (TE)-like cells (TELCs) and trophoblast stem cells (TSCs), offering a valuable in vitro model to study early placenta specification. Here, we demonstrate that the VGLL1 (vestigial-like family member 1), which is highly expressed during human and non-human primate TE specification in vivo but is negligibly expressed in mouse, is a critical regulator of cell fate determination and self-renewal in human TELCs and TSCs derived from naïve PSCs. Mechanistically, VGLL1 partners with the transcription factor TEAD4 (TEA domain transcription factor 4) to regulate chromatin accessibility at target gene loci through histone acetylation and acts in cooperation with GATA3 and TFAP2C. Our work is relevant to understand primate early embryogenesis and how it differs from other mammalian species.

| S-EPMC10794710 | biostudies-literature

Author Correction: VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification.

Project description: Not available

| S-EPMC11920433 | biostudies-literature

VGLL1 regulates extraembryonic lineage specification in human [RNA-Seq]

Project description:Placenta abnormality is one of the key reasons for early pregnancy loss but the regulatory mechanisms underlying placenta formation are largely unknown. Here, we applied a human naïve pluripotent stem cell (PSC) derived TE model to explore the driven regulatory machinery. We demonstrate that VGLL1 (vestigial like family member 1) is crucial for TE self-renewal and TE-specific gene expression, thus suppressing VGLL1 leads to severely impaired cell proliferation and skewed TE induction. VGLL1 exerts its function through interacting with TEAD4 (TEA domain transcription factor 4) and colocalize at target gene promoters and enhancers. Further investigation uncovers the enrichment of H3K27ac active histone marks at genomic regions occupied by VGLL1-TEAD4 complex, indicates a close association between them. Overall, our data reveals the critical function model of VGLL1-TEAD4 in human TE derivation, highlighting a potential interspecies difference between human and mouse TE induction.

2023-12-18 | GSE193619 | GEO

VGLL1 regulates extraembryonic lineage specification in human [CUT&TAG]

2023-12-18 | GSE193618 | GEO

VGLL1 regulates extraembryonic lineage specification in human [ATAC-Seq]

2023-12-18 | GSE193612 | GEO

VGLL1 regulates extraembryonic lineage specification in human [RNA-seq II]

Project description:Placenta abnormality is one of the key reasons for early pregnancy loss but the regulatory mechanisms underlying placenta formation are largely unknown. Here, we applied a human naïve pluripotent stem cell (PSC) derived TE model to explore the driven regulatory machinery. We demonstrate that VGLL1 (vestigiallikefamilymember1) is crucial for TE self-renewal and TE-specific gene expression, thus suppressing VGLL1 leads to severely impaired cell proliferation and skewed TE induction. VGLL1 exerts its function through interacting with TEAD4 (TEA domain transcription factor 4) and colocalize at target gene promoters and enhancers. Further investigation uncovers the enrichment of H3K27ac active histone marks at genomic regions occupied by VGLL1-TEAD4 complex, indicates a close association between them. Overall, our data reveals the critical function model of VGLL1-TEAD4 in human TE derivation, highlighting a potential interspecies difference between human and mouse TE induction.

2023-12-18 | GSE241813 | GEO

VGLL1 cooperates with TEAD4 to control human trophectoderm lineage specification

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

2023-12-16 | GSE193621 | GEO

Altered Subcellular Localization of Transcription Factor TEAD4 Regulates First Mammalian Cell Lineage Commitment

Project description:In the preimplantation mouse embryo TEAD4 is critical to establishing the trophectoderm (TE)-specific transcriptional program and segregating TE from the inner cell mass (ICM). However, TEAD4 is expressed both in the TE and the ICM. Thus, differential function of TEAD4 rather than expression itself regulates specification of the first two cell lineages. We used ChIP-seq to define genome-wide TEAD4 target genes and asked how transcription of TEAD4 target genes is specifically maintained in the TE. Our analyses revealed an evolutionarily conserved mechanism, in which lack of nuclear localization of TEAD4 impairs the TE-specific transcriptional program in inner blastomeres, thereby allowing their maturation towards the ICM lineage. Restoration of TEAD4 nuclear localization maintains the TE-specific transcriptional program in the inner blastomeres and prevents segregation of the TE and ICM lineages and blastocyst formation. We propose that altered subcellular localization of TEAD4 in blastomeres dictates first mammalian cell fate specification. ChIPseq profiles of TEAD4, IgG, Input in Mouse trophoblast stem cells using Illumina HiSeq 2000 and Illumina Genome Analyzer IIx

2012-04-18 | E-GEOD-37350 | biostudies-arrayexpress

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