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Chicken neural crest and neural plate

ABSTRACT: Neural cest cells are a transient stem cell-like population appearing during vertebrate embryonic development. Generation of the cranial neural crest is known to require a balanced combination of FGF and BMP levels. However, it is poorly understood how the functions of such growth factors are controlled in the extracellular spaces. Anosmin is an extracellular matrix protein implicated in FGF signaling and mutated in Kallmann syndrome. Here, we demonstrate that anosmin (Gga.14976.1.S1_at, clone ChEST132d10) is synthesized locally in the cranial neural crest of chicken embryos and is essential for cranial neural crest formation. Anosmin upregulates FGF8 and BMP5 gene expression; it also enhances FGF8 activity while inhibiting BMP5 and WNT3a signaling. Taken together, our data establish that the matrix protein anosmin is required for cranial neural crest formation, with funtional modulation of FGF, BMP, and WNT.

ORGANISM(S): Gallus gallus

PROVIDER: GSE38381 | GEO | 2012/06/01

SECONDARY ACCESSION(S): PRJNA167793

REPOSITORIES: GEO

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Chicken neural crest and neural plate

Project description:Neural cest cells are a transient stem cell-like population appearing during vertebrate embryonic development. Generation of the cranial neural crest is known to require a balanced combination of FGF and BMP levels. However, it is poorly understood how the functions of such growth factors are controlled in the extracellular spaces. Here we identifiy the extracelluar matrix protein anosmin (Gga.14976.1.S1_at, clone ChEST132d10) as a novel molecule synthesized locally in the cranial neural crest of chicken embryos. Cranial neural folds (NF) and ventral neural plates (NP) were dissected from Hamburger & Hamilton stage 8 (HH8) embryos (80 to 14 embryos, n=4), and total RNA was analyzed using a GeneChip chicken genome arrays (Affymetrix)

2012-05-31 | E-GEOD-38381 | biostudies-arrayexpress

DAN (NBL1) promotes collective neural crest migration by restraining uncontrolled invasion

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Project description:We employ RNA-seq of FACS sorted cell populations to identify genes that are enriched in cranial neural crest in relationship to the trunk. Transcriptional profiling of delaminating cranial and trunk neural crest subpopulations.

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Fgf8 signaling alters the osteogenic cell fate in anterior hard palate

Project description:FGF signaling has been implicated in the regulation of osteogenesis in both intramembranous and endochondral ossification. In the developing palate, the anterior bony palate forms by direct differentiation of cranial neural crest-derived mesenchymal cells, but the signals that regulate osteogenic cell fate remains unclear. In the present study, we present evidence that locally activated FGF8 signaling in the anterior palate leads to complete bone loss of the palatine process of the maxilla (ma) and ectopic cartilage formation. This aberrant developmental process was accompanied by significantly elevated level of cell proliferation, which contributes to abnormally thickened ma, and complete inhibition of Osterix expression, which accounts for the lack of bone formation. Consistent with the phenotype, RNA-Sequencing (RNA-Seq) analysis further demonstrated that augmented FGF8 signaling downregulated genes involved in ossification, biomineral tissue development, and bone mineralization, but upregulated genes involved in cell proliferation, cartilage development, and cell fate commitment. Expression validation of selected genes supported the RNA-Seq results. We conclude that FGF signaling functions as a negative regulator of osteogenic fate but promotes chondrogenesis of cranial neural crest cell-derived mesenchyme in the hard palate, which will have implication in directed differentiation of precursor cells for clinical application.

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A chemical screen in zebrafish embryonic cells establishes that Akt activation is required for neural crest development [ATAC-seq]

Project description:The neural crest is a dynamic progenitor cell population that arises at the border of neural and non-neural ectoderm. The inductive roles of FGF, Wnt, and BMP at the neural plate border are well established, but the signals required for subsequent neural crest development remain poorly characterized. Here, we conducted a screen in primary zebrafish embryo cultures for chemicals that decrease neural crest formation, as read out by crestin:EGFP expression. We found that the natural product caffeic acid phenethyl ester (CAPE) disrupts neural crest gene expression, migration, and melanocytic differentiation by reducing Sox10 activity. CAPE inhibits PI3K/Akt signaling specifically in FGF-stimulated cells, and neural crest defects in CAPE-treated embryos are suppressed by constitutively active Akt1. Inhibition of Akt activity by constitutively active PTEN similarly decreases crestin expression and Sox10 activity. Our study has identified Akt as a novel intracellular pathway required for neural crest development.

2017-08-17 | GSE95813 | GEO

A chemical screen in zebrafish embryonic cells establishes that Akt activation is required for neural crest development [RNA-seq]

2017-08-17 | GSE95814 | GEO

Post-transcriptional regulation in cranial neural crest cells expands developmental potential [I]

Project description:Developmental potential is progressively restricted after germ layer specification during gastrulation. However, cranial neural crest cells challenge this paradigm, as they develop from anterior ectoderm yet give rise to both mesodermal derivatives of the craniofacial skeleton and ectodermal derivatives of the peripheral nervous system. How cranial neural crest cells differentiate into multiple lineages is poorly understood. Here, we demonstrate that cranial neural crest cells possess a transient state of increased chromatin accessibility; and that the earliest premigratory neural crest are biased towards either a neuronal or ectomesenchymal fate, with each lineage expressing distinct factors from the pluripotent state. We profile the spatiotemporal emergence of each neural crest population and demonstrate that the ectomesenchymal lineage forms prior to the neuronal progenitors. Expression of the pluripotency microRNA family miR-302 is maintained in cranial neural crest cells and genetic deletion leads to precocious specification of the ectomesenchymal lineage. We find that miR-302 directly targets Sox9 to slow the timing of ectomesenchyme induction and regulates multiple genes involved in chromatin condensation to maintain accessibility for neuronal differentiation. Loss of mir-302 results in reduced chromatin accessibility in the neuronal progenitor lineage of neural crest and a reduction in peripheral neuron differentiation. Our findings reveal a post-transcriptional mechanism governed by miRNAs from pluripotency as an important mechanism to expand developmental potential of cranial neural crest.

2022-10-25 | GSE215977 | GEO

Post-transcriptional regulation in cranial neural crest cells expands developmental potential [II]

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Neural crest cells bulldoze through the microenvironment using water channel proteins to stabilize filopodia

Project description:Neural crest migration requires cells to move through dense extracellular matrix and mesoderm to reach targets throughout the vertebrate embryo. Here, we use high-resolution microscopy, computational modeling, and in vitro and in vivo cell invasion assays to investigate the function of Aquaporin-1 (AQP-1) signaling. We find that migrating cranial neural crest cells express AQP-1 mRNA and protein within cell filopodia, implicating a biological role for water channel protein function during invasion. Differential AQP-1 levels affect neural crest cell speed, direction, and the length and stability of cell filopodia. Further, AQP-1 enhances matrix metalloprotease (MMP) activity and phosphorylated focal adhesion kinases (pFAK). Co-localization of AQP-1 expression with EphB guidance receptors in the same migrating neural crest cells raises novel implications for the concept of guided bulldozing by lead cells during migration.

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