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Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE236796 | GEO | 2024/03/11

REPOSITORIES: GEO

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Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements [RNA-seq]

Project description:The commitment and differentiation of human placental progenitor cytotrophoblast (CT) cells are crucial for a successful pregnancy, but the underlying regulatory mechanism remains poorly understood. Here we identified the transcription factor (TF), Specificity protein 6 (SP6), as a human species-specific trophoblast lineage TF expressed in human placental CT cells. Using pluripotent stem cells as a model, we demonstrated that SP6 governs CT generation and the establishment of trophoblast stem cells (TSCs) and discovered msh homeobox 2 (MSX2) as the downstream effector in these events. Mechanistically, we showed that SP6 interacts with histone acetyltransferase P300 to modulate the landscape of H3K27ac at targeted regulatory elements, thereby favoring transcriptional activation and facilitating CT cell fate decisions and TSC maintenance. Our results established SP6 as a novel regulator of the human trophoblast lineage and implied its regulatory role in placental development and the pathogenies of placental diseases.

2024-03-11 | GSE236795 | GEO

Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements [ChIP-seq]

2024-03-11 | GSE236794 | GEO

Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements

Project description:Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements

| PRJNA992434 | ENA

Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements [RNA-seq]

Project description:Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements [RNA-seq]

| PRJNA992440 | ENA

Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements [ChIP-seq]

Project description:Specificity protein 6 governs human cytotrophoblast fate decisions and trophoblast stem cell establishment by targeting MSX2 regulatory elements [ChIP-seq]

| PRJNA992441 | ENA

MSX2 safeguards syncytiotrophoblast fate of human trophoblast stem cells.

Project description:Multiple placental pathologies are associated with failures in trophoblast differentiation, yet the underlying transcriptional regulation is poorly understood. Here, we discovered msh homeobox 2 (MSX2) as a key transcriptional regulator of trophoblast identity using the human trophoblast stem cell model. Depletion of MSX2 resulted in activation of the syncytiotrophoblast transcriptional program, while forced expression of MSX2 blocked it. We demonstrated that a large proportion of the affected genes were directly bound and regulated by MSX2 and identified components of the SWItch/Sucrose nonfermentable (SWI/SNF) complex as strong MSX2 interactors and target gene cobinders. MSX2 cooperated specifically with the SWI/SNF canonical BAF (cBAF) subcomplex and cooccupied, together with H3K27ac, a number of differentiation genes. Increased H3K27ac and cBAF occupancy upon MSX2 depletion imply that MSX2 prevents premature syncytiotrophoblast differentiation. Our findings established MSX2 as a repressor of the syncytiotrophoblast lineage and demonstrated its pivotal role in cell fate decisions that govern human placental development and disease.

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MSX2 in ameloblast cell fate and activity.

Project description:While many effectors have been identified in enamel matrix and cells via genetic studies, physiological networks underlying their expression levels and thus the natural spectrum of enamel thickness and degree of mineralization are now just emerging. Several transcription factors are candidates for enamel gene expression regulation and thus the control of enamel quality. Some of these factors, such as MSX2, are mainly confined to the dental epithelium. MSX2 homeoprotein controls several stages of the ameloblast life cycle. This chapter introduces MSX2 and its target genes in the ameloblast and provides an overview of knowledge regarding its effects in vivo in transgenic mouse models. Currently available in vitro data on the role of MSX2 as a transcription factor and its links to other players in ameloblast gene regulation are considered. MSX2 modulations are relevant to the interplay between developmental, hormonal and environmental pathways and in vivo investigations, notably in the rodent incisor, have provided insight into dental physiology. Indeed, in vivo models are particularly promising for investigating enamel formation and MSX2 function in ameloblast cell fate. MSX2 may be central to the temporal-spatial restriction of enamel protein production by the dental epithelium and thus regulation of enamel quality (thickness and mineralization level) under physiological and pathological conditions. Studies on MSX2 show that amelogenesis is not an isolated process but is part of the more general physiology of coordinated dental-bone complex growth.

| S-EPMC4283505 | biostudies-literature

Targeting a major hub of cell fate decisions - the mitochondrial-associated membrane.

Project description: Not available

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Meigo governs dendrite targeting specificity by modulating ephrin level and N-glycosylation.

Project description:Neural circuit assembly requires precise dendrite and axon targeting. We identified an evolutionarily conserved endoplasmic reticulum (ER) protein, Meigo, from a mosaic genetic screen in Drosophila melanogaster. Meigo was cell-autonomously required in olfactory receptor neurons and projection neurons to target their axons and dendrites to the lateral antennal lobe and to refine projection neuron dendrites into individual glomeruli. Loss of Meigo induced an unfolded protein response and reduced the amount of neuronal cell surface proteins, including Ephrin. Ephrin overexpression specifically suppressed the projection neuron dendrite refinement defect present in meigo mutant flies, and ephrin knockdown caused a similar projection neuron dendrite refinement defect. Meigo positively regulated the level of Ephrin N-glycosylation, which was required for its optimal function in vivo. Thus, Meigo, an ER-resident protein, governs neuronal targeting specificity by regulating ER folding capacity and protein N-glycosylation. Furthermore, Ephrin appears to be an important substrate that mediates Meigo's function in refinement of glomerular targeting.

| S-EPMC4779446 | biostudies-literature

Establishment of bovine trophoblast stem cells.

Project description:Here, we report that a chemical cocktail (LCDM: leukemia inhibitory factor [LIF], CHIR99021, dimethinedene maleate [DiM], minocycline hydrochloride), previously developed for extended pluripotent stem cells (EPSCs) in mice and humans, enables de novo derivation and long-term culture of bovine trophoblast stem cells (TSCs). Bovine TSCs retain developmental potency to differentiate into mature trophoblast cells and exhibit transcriptomic and epigenetic (chromatin accessibility and DNA methylome) features characteristic of trophectoderm cells from early bovine embryos. The bovine TSCs established in this study will provide a model to study bovine placentation and early pregnancy failure.

| S-EPMC10950030 | biostudies-literature

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