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Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [RNA-seq]

ABSTRACT: Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [RNA-seq]

PROVIDER: PRJNA907858 | ENA |

REPOSITORIES: ENA

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Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development

Project description:Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development

| PRJNA911737 | ENA

Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [ChIP-seq]

Project description:Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [ChIP-seq]

| PRJNA907861 | ENA

Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [scRNA-seq]

Project description:Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [scRNA-seq]

| PRJNA911734 | ENA

Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [scRNA-seq]

Project description:As ontogeny does not recapitulate phylogeny and little developmental restraint exists prior to gastrulation, early mammalian development differs significantly between species. A prime example is the temporal difference in the first emergence of extra-embryonic mesenchymal cells (ExMC) between mouse and human. Here, we report a fast and efficient in vitro cell model of human ExMC formation from induced pluripotent stem cells. This ExMC emerges from the apparent late blastocystic trophoblast. We define HAND1 as an essential regulator of ExMC specification, with HAND1 null cells reverting to the trophoblast lineage. Regulatory phenotyping defines primary target genes of, and primate-specific genomic regions bound by, HAND1. These data emphasize the nascent evolutionary innovation in early development relevant to human health but, through pleiotropy, also to later in life human biology. The novel findings that trophectoderm is a source of ExMC lineage and how recently evolved young transposable elements regulate this process emphasize the evolutionary novelties of our model to explore the primate embryogenesis.

2024-12-02 | GSE220840 | GEO

Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [ChIP-seq]

2024-12-02 | GSE219291 | GEO

Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development [RNA-seq]

2024-12-02 | GSE219290 | GEO

Origin of extra-embryonic mesenchyme points to evolutionary novelty in primate early development

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

2024-12-02 | GSE220844 | GEO

Linum usitatissimum cultivar:Novelty

Project description:Linum usitatissimum cultivar:Novelty Genome sequencing

| PRJNA1061538 | ENA

Primary mouse embryonic palatal mesenchyme LC-MS/MS

Project description:To identify proteins phosphorylated by Akt downstream of PI3K-mediated PDGFRalpha signaling, we immunoprecipitated Akt phosphorylation substrates from PDGF-AA-treated primary mouse embryonic palatal mesenchyme (MEPM) lysates and analyzed the peptides by nano LC-MS/MS.

2019-06-04 | PXD000779 | Pride

GPR158 in pyramidal neurons mediates social novelty behavior via modulating synaptic transmission in male mice

Project description:Impairment in social communication skills is a hallmark feature of autism spectrum disorder (ASD). The role of G-protein coupled receptor 158 (GPR158) in ASD remains largely unexplored. In this study, we observed both constitutive and cell/tissue-specific knockouts of Gpr158 in pyramidal neurons or medial prefrontal cortex (mPFC) result in impaired novelty preference, while sociability remains unaffected in male mice. Notably, loss of GPR158 leads to a significant decline in excitatory synaptic transmission, characterized by the reduction in glutamate vesicles, as well as the expression and phosphorylation of GluN2B in the mPFC. We successfully rescue the phenotype of social novelty deficits either by reintroducing GPR158 in the mPFC of Gpr158 deficient mice or by chemogenetic activation of pyramidal neurons where Gpr158 is specifically ablated. Our findings indicate that GPR158 in pyramidal neurons plays a specific role in modulating social novelty, and may represent a potential target for treating social disorder.

2024-09-04 | GSE276304 | GEO

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