Gallus gallus
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ABSTRACT:
PROVIDER: PRJNA322350 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptome profiling reveals BMP target genes during midbrain neural crest delamination
| PRJNA717985 | ENA
Project description:During embryonic development, the neural crest is a transient, migratory cell population that differentiates into a large variety of tissues and contributes much to the formation of vertebrate body. In Xenopus, lrig3 is involved in neural crest formation by modulating FGF and Wnt signaling. Lrig3 functions downstream of pax3 and zic1 to regulate the expression of neural crest markers. We used microarrays to identify the lrig3 target genes during neural crest formation.
2014-09-01 | GSE50487 | GEO
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 a timecourse of Dual SMAD Inhibition (DSi), Neural Crest (NC), and Melanocyte (BE) differentiation of human embryonic stem cells in triplicate.
2013-06-01 | E-GEOD-45223 | biostudies-arrayexpress
Project description:Cardiac and trunk neural crest transcriptome comparison
| PRJNA515142 | ENA
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.
2013-06-01 | E-GEOD-45226 | biostudies-arrayexpress
Project description:The process of cell fate commitment requires sequential changes in the gene expression profiles of embryonic progenitors. This is exemplified in the development of the neural crest, a migratory stem cell population derived from the ectoderm of vertebrate embryos. Neural crest formation involves a series of regulatory changes, in which cells adopt distinct transcriptional states in a stepwise manner. The mechanisms underpinning these shifts in cell identity are still poorly understood. Here we employ enhancer analysis to identify a genetic sub-circuit that controls developmental transitions in neural crest development. This sub-circuit links Wnt target genes in an incoherent forward loop that controls the sequential activation of genes in the neural crest lineage. By examining the cis-regulatory apparatus of Wnt effector gene AXUD1, we found that multipotency factor SP5 directly promotes neural plate border identity, while inhibiting premature specification by interacting with tissue specific enhancers.
2020-12-17 | GSE152599 | GEO
Project description:Transcriptional profile of the migratory cardiac neural crest
| PRJNA492347 | ENA
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. 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.
2012-06-01 | GSE38381 | GEO
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.
2022-01-01 | GSE125140 | GEO