RNA Sequencing of default, melanocyte biased and enteric human neural crest populations (NC) and neuroectoderm (CNS)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE66148 | GEO | 2016/02/12
SECONDARY ACCESSION(S): PRJNA278733
REPOSITORIES: GEO
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Project description:We have generated expression profiles of three different neural crest populations from human embryonic stem cells. These profiles were compared to a neuroectoderm population. We find that the neural crest populations are separable and distinct. All cell types were differentiated from human embryonic stem cells. Neural crest populations were sorted on day 12 for CD49. The neuroectoderm cells were unsorted and harvested on day 12 of differentiation.
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Project description:Melanocytes are pigment-producing cells of neural crest origin responsible for protecting the skin against UV-irradiation. Melanocyte dysfunction leads to pigmentation defects including albinism, vitiligo, and piebaldism and is a key feature of systemic pathologies such as Hermansky-Pudlak (HP) and Chediak-Higashi (CH) Syndromes. Pluripotent stem cell technology offers a novel approach for studying human melanocyte development and disease. Here we report that timed exposure to activators of WNT, BMP and EDN3 signaling triggers the sequential induction of neural crest and melanocyte precursor fates under dual-SMAD inhibition conditions. Using a SOX10::GFP hESC reporter line, we demonstrate that the temporal onset of WNT activation is particularly critical for human neural crest induction. Surprisingly, suppression of BMP signaling does reduce neural crest yield. Subsequent differentiation of hESC-derived melanocyte precursors under defined conditions yields pure populations of pigmented cells matching the molecular and functional properties of adult melanocytes. Melanocytes from patient-specific iPSCs faithfully reproduce the ultrastructural features of the HP- and CH-specific pigmentation defects with minimal variability across lines. Our data define a highly specific requirement for WNT signaling during neural crest induction and enable the generation of pure populations of hiPSC-derived melanocytes for faithful modeling of human pigmentation disorders. Total RNA obtained from embryonic stem cells (ESCs), ESC-derived melanocyte progenitors, ESC-derived mature melanocytes, primary melanocytes, and disease-specific induced pluripotent stem cell-derived melanocytes.
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Project description:Human neural crest cell development progresses via a pre-neural border (pNB) cell state that precedes the induction of the neurectoderm and the neural border. Here, we identify a set of pNB gene candidates, including forkhead box B1 (FOXB1), and their associated enhancers, that are rapidly activated by β-catenin-mediated signaling during human embryonic stem (ES) cell differentiation towards neural crest cells. FOXB1 simultaneously maintains neuroectoderm competency and controls the timing of differentiating ES cells to acquire neural crest fate by directly targeting key neural crest and neural progenitor loci in a context-dependent manner. Notably, the transient expression of FOXB1 in pre-neural crest cells also establishes autonomic neurogenic potential in mature neural crest cells, likely via its regulation of the expression of ASCL1, a master regulator of autonomic neurons. Altogether, our data implicates pNB cell state as the missing link bridging the exit of pluripotency to the acquisition of neural crest fate and its diverse ecto-mesenchymal differentiation potentials.
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Project description:Human neural crest cell development progresses via a pre-neural border (pNB) cell state that precedes the induction of the neurectoderm and the neural border. Here, we identify a set of pNB gene candidates, including forkhead box B1 (FOXB1), and their associated enhancers, that are rapidly activated by β-catenin-mediated signaling during human embryonic stem (ES) cell differentiation towards neural crest cells. FOXB1 simultaneously maintains neuroectoderm competency and controls the timing of differentiating ES cells to acquire neural crest fate by directly targeting key neural crest and neural progenitor loci in a context-dependent manner. Notably, the transient expression of FOXB1 in pre-neural crest cells also establishes autonomic neurogenic potential in mature neural crest cells, likely via its regulation of the expression of ASCL1, a master regulator of autonomic neurons. Altogether, our data implicates pNB cell state as the missing link bridging the exit of pluripotency to the acquisition of neural crest fate and its diverse ecto-mesenchymal differentiation potentials.
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Project description:Human neural crest cell development progresses via a pre-neural border (pNB) cell state that precedes the induction of the neurectoderm and the neural border. Here, we identify a set of pNB gene candidates, including forkhead box B1 (FOXB1), and their associated enhancers, that are rapidly activated by β-catenin-mediated signaling during human embryonic stem (ES) cell differentiation towards neural crest cells. FOXB1 simultaneously maintains neuroectoderm competency and controls the timing of differentiating ES cells to acquire neural crest fate by directly targeting key neural crest and neural progenitor loci in a context-dependent manner. Notably, the transient expression of FOXB1 in pre-neural crest cells also establishes autonomic neurogenic potential in mature neural crest cells, likely via its regulation of the expression of ASCL1, a master regulator of autonomic neurons. Altogether, our data implicates pNB cell state as the missing link bridging the exit of pluripotency to the acquisition of neural crest fate and its diverse ecto-mesenchymal differentiation potentials.
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