Gallus gallus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA302598 | ENA |
REPOSITORIES: ENA
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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.
2016-06-24 | E-GEOD-75125 | biostudies-arrayexpress
Project description:The cranial neural crest (CNC) is a vertebrate-specific population that generates a huge diversity of derivatives, including the bulk of the connective and skeletal tissues of the head. How neural crest cells generate the appropriate cell types for distinct head regions over time remains unresolved. Here we profile RNA expression (scRNAseq) and chromatin accessibility (snATACseq) of the zebrafish cranial neural crest lineage at single-cell resolution from embryos to adults.
2021-11-11 | GSE178969 | GEO
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tongue development in order to study the contribution of cranial neural crest (CNC) cells towards the patterning of cranial mesoderm for proper tongue formation. Here, we conducted gene expression profiling of embryonic tongue tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of microglossia, a common congenital birth defect which is frequently observed with several syndromic conditions. To investigate the mechanism of microglossia resulting from dysfunctional TGF-Beta signaling during muscle development, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses of tongue tissue of Tgfbr2fl/fl;Wnt1-Cre mutant mice and Tgfbr2fl/fl control mice at embryonic day E14.5 (n=3 per genotype) to examine the genes regulated by Tgf-beta during tongue muscle development.
2013-04-11 | E-GEOD-45968 | biostudies-arrayexpress
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have used Next-Generation sequencing to profile all 20-40nt microRNAs from micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks). Samples for each species were isolated at two developmental stages, before (Hamilton Hamburger stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Examination of microRNA expression in frontonasal neural crest cells of 3 bird species at two developmental stages. Includes some biological replicates and one technical replicate.
2012-05-02 | E-GEOD-30716 | biostudies-arrayexpress
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 | GSE216136 | GEO
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
Project description:The cranial neural crest cells are pluripotent cells that provide head skeletogenic mesenchyme and are crucial for craniofacial patterning. Here, we analyzed the in vivo chromatin landscapes of mouse cranial neural crest subpopulations. Early postmigratory neural crest subpopulations contributing to distinct mouse craniofacial structures displayed similar chromatin accessibility patterns, yet differed transcriptionally. Accessible promoters and enhancers of differentially silenced genes carried H3K27me3/H3K4me2 bivalent chromatin marks embedded in large Ezh2-dependent Polycomb domains, indicating transcriptional poising. These postmigratory bivalent regions were already present in neural crest premigratory progenitors. At Polycomb domains, H3K27me3 antagonized H3K4me2 deposition, which was restricted to accessible sites. Thus, bivalent Polycomb domains provide a chromatin template for the regulation of cranial neural crest cell positional identity in vivo contributing novel insights into the epigenetic regulation of face morphogenesis.
2017-03-31 | GSE89434 | GEO