Directed differentiation of placode from human embryonic stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51533 | GEO | 2013/12/04
SECONDARY ACCESSION(S): PRJNA223384
REPOSITORIES: GEO
Similar Datasets
Project description:Here we compare the transcriptional profile during the differentiation of hESC into neuroepithelial cells (NSB) (Chambers et. al 2009 Nature Biotechnology) with our new placode differentiation (PIP). Total RNA was isolated at day 1,3, 5 (NSB), 5 (PIP), 7 (NSB), 7 (PIP), 9 (NSB), 9 (PIP), 11 (NSB) and 11 (PIP) of differentiation using Trizol. Samples for each group in triplicate were processed for Illumina bead arrays (Illumina HT-12) by the MSKCC genomics core facility according to the specifications of the manufacturer.
2013-12-04 | E-GEOD-51533 | biostudies-arrayexpress
Project description:The inner ear develops from a patch of thickened cranial ectoderm adjacent to the hindbrain called the otic placode. Studies in a number of vertebrate species suggest that the initial steps in induction of the otic placode are regulated by members of the Fibroblast Growth Factor (FGF) family, and that inhibition of FGF signaling can prevent otic placode formation. To better understand the genetic pathways activated by FGF signaling during otic placode induction, we performed microarray experiments to estimate the proportion of chicken otic placode genes that can be up-regulated by the FGF pathway in a simple culture model of otic placode induction. Surprisingly, we find that FGF is only sufficient to induce about 15% of chick otic placode-specific genes in our experimental system. However, pharmacological blockade of the FGF pathway in cultured chick embryos showed that although FGF signaling was not sufficient to induce the majority of otic placode-specific genes, it was still necessary for their expression in vivo. These inhibitor experiments further suggest that the early steps in otic placode induction regulated by FGF signaling occur through the MAP kinase pathway. Although our work suggests that FGF signaling is necessary for otic placode induction, it demonstrates that other unidentified signaling pathways are required to co-operate with FGF signaling to induce the full otic placode program.
2012-12-12 | GSE42845 | GEO
Project description:The inner ear develops from a patch of thickened cranial ectoderm adjacent to the hindbrain called the otic placode. Studies in a number of vertebrate species suggest that the initial steps in induction of the otic placode are regulated by members of the Fibroblast Growth Factor (FGF) family, and that inhibition of FGF signaling can prevent otic placode formation. To better understand the genetic pathways activated by FGF signaling during otic placode induction, we performed microarray experiments to estimate the proportion of chicken otic placode genes that can be up-regulated by the FGF pathway in a simple culture model of otic placode induction. Surprisingly, we find that FGF is only sufficient to induce about 15% of chick otic placode-specific genes in our experimental system. However, pharmacological blockade of the FGF pathway in cultured chick embryos showed that although FGF signaling was not sufficient to induce the majority of otic placode-specific genes, it was still necessary for their expression in vivo. These inhibitor experiments further suggest that the early steps in otic placode induction regulated by FGF signaling occur through the MAP kinase pathway. Although our work suggests that FGF signaling is necessary for otic placode induction, it demonstrates that other unidentified signaling pathways are required to co-operate with FGF signaling to induce the full otic placode program.
2012-12-12 | GSE42845 | GEO
Project description:The inner ear develops from a patch of thickened cranial ectoderm adjacent to the hindbrain called the otic placode. Studies in a number of vertebrate species suggest that the initial steps in induction of the otic placode are regulated by members of the Fibroblast Growth Factor (FGF) family, and that inhibition of FGF signaling can prevent otic placode formation. To better understand the genetic pathways activated by FGF signaling during otic placode induction, we performed microarray experiments to estimate the proportion of chicken otic placode genes that can be up-regulated by the FGF pathway in a simple culture model of otic placode induction. Surprisingly, we find that FGF is only sufficient to induce about 15% of chick otic placode-specific genes in our experimental system. However, pharmacological blockade of the FGF pathway in cultured chick embryos showed that although FGF signaling was not sufficient to induce the majority of otic placode-specific genes, it was still necessary for their expression in vivo. These inhibitor experiments further suggest that the early steps in otic placode induction regulated by FGF signaling occur through the MAP kinase pathway. Although our work suggests that FGF signaling is necessary for otic placode induction, it demonstrates that other unidentified signaling pathways are required to co-operate with FGF signaling to induce the full otic placode program. 8 samples were analyzed. These contain two replicates of each of the following four catergories: Otic ectoderm, Non-Otic (lateral) ectoderm, Trigeminal Ectoderm cultured - FGF, Trigeminal Ectoderm cultured + FGF
2012-12-12 | E-GEOD-42845 | biostudies-arrayexpress
Project description:Here we compare the transcriptional profile of neural crest cells differentiated on MS5 feeder cells (Lee et al., 2007 Nature Biotechnology) with neural crest cells differentiated in a feeder-free protocol. As controls, neuroepithelial cells (LSB) and wnt-induced neural crest cells were included.
2014-12-31 | GSE50643 | GEO
Project description:In mouse early organogenic stages, a Mab21l1-null mutation causes severe defects in invagination of the lens placode toward optic cup due to its severe defects in both cell proliferation and survival, which subsequently results in severe microphthalmia after birth. In human, loss of function variants in MAB21L1 have recently been described in Cerebello-Oculo-Facio-Genital syndrome (COFG syndrome). The close similarity between mouse and human phenotypes including microphthalmia indicates the importance of Mab21l1 function in human lens placode. To approach the molecular function of MAB21L1 in eye morphogenesis, we examined single cell transcriptomes in lens placode and its surrounding surface ectoderm at 26 somite stage (E9.25), just prior to the onset of lens defects in Mab21l1-null embryos. Here we demonstrate the identification of several key genes immediately downstream of Mab21l1 function, together with the early lens placode-/surface ectoderm-specific single cell transcriptomes during murine lens placode specification.
2021-11-30 | GSE167126 | GEO
Project description:Few families of signaling factors have been implicated in the control of development. Here we identify the neuropeptides nociceptin and somatostatin, a neurotransmitter and neuroendocrine hormone, as a class of developmental signals in chick and zebrafish. We show that signals from the anterior mesendoderm are required for the formation of anterior placode progenitors with one of the signals being somatostatin. Somatostatin controls ectodermal expression of nociceptin and both peptides regulate Pax6 in lens and olfactory progenitors. Consequently, loss of somatostatin and nociceptin signaling leads to severe reduction of lens formation. Our findings not only uncover these neuropeptides as developmental signals, but also identify a long-sought-after mechanism that initiates Pax6 in placode progenitors and may explain the ancient evolutionary origin of neuropeptides, pre-dating a complex nervous system. We used progenitors for anterior and posterior sensory placodes dissected from chick embryos HH5-7; these were either processed immediately or cultured for 5 hrs to hybridise to Affymetrix chick array. We aimed to identify genes that are co regualted with Pax6, a key regulator of lens and olfactory progenitor cells. Pax6 is normally present in anterior, but not posterior placode precursors, but upregulated in both after 5 hrs culture.
2014-04-25 | E-GEOD-48116 | biostudies-arrayexpress
Project description:Cranial placodes contribute to all sense organs and sensory ganglia in the vertebrate head. Despite their diversity they originate from a common pool of Six1/Eya2+ progenitors. In a molecular screen we identify new factors upstream of the Six1/Eya2 cassette and use these to dissect the transcriptional hierarchy that controls progenitor specification. We find that although two different tissues, the lateral head mesoderm and the prechordal mesendoderm, induce placode progenitors, both initiate a common transcriptional state, but over time gradually impart regional character. Thus, as cells acquire placode progenitor identify they pass through successive transcriptional states each identified by a distinct set of factors and controlled by different signalling pathways. Thus, we propose a new model for placode progenitor induction reminiscent of Waddington’s evocation-individuation model for neural induction.
2017-07-12 | GSE81023 | GEO
Project description:Few families of signaling factors have been implicated in the control of development. Here we identify the neuropeptides nociceptin and somatostatin, a neurotransmitter and neuroendocrine hormone, as a class of developmental signals in chick and zebrafish. We show that signals from the anterior mesendoderm are required for the formation of anterior placode progenitors with one of the signals being somatostatin. Somatostatin controls ectodermal expression of nociceptin and both peptides regulate Pax6 in lens and olfactory progenitors. Consequently, loss of somatostatin and nociceptin signaling leads to severe reduction of lens formation. Our findings not only uncover these neuropeptides as developmental signals, but also identify a long-sought-after mechanism that initiates Pax6 in placode progenitors and may explain the ancient evolutionary origin of neuropeptides, pre-dating a complex nervous system.
2014-04-25 | GSE48116 | GEO
Project description:In this setup gene profiling of hair follicle keratinocytes with active nuclear NF-κB is used to further analyze the role of NF-κB in HF development. For this purpose an NF-κB-responsive EGFP reporter mouse has been constructed, which enables in vivo visualization of cells with NF-κB activity and their isolation via fluorescence assisted cell sorting (FACS). The isolated cells were used to establish a gene profile of early hair placode keratinocytes with NF-κB activity (E14.5).
2016-02-29 | E-MTAB-4535 | biostudies-arrayexpress