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Gene expression of differentiating hESCs into otic progenitors

ABSTRACT: Stem cells, with their potential to generate different lineages, could offer a solution by replacing damaged or lost cells within the inner ear. We have shown that human embryonic stem cells can be induced to differentiate into otic progenitors, and then into hair cell-like cells and neurons that display expected electrophysiological properties. More importantly, once these otic progenitors are transplanted into animals with induced hearing loss, they differentiate and elicit a significant recovery of auditory function. The generation of otic progenitors is triggered by FGF signalling. In this dataset we have analysed the global gene expression profile of undifferentiated hESCs and compared with cultures that have been treated with FGF3 and 10, the two ligands involved in otic induction, or cultures that have been allowed to differentiate under basal conditions without FGF (DFNB).

ORGANISM(S): Homo sapiens

PROVIDER: GSE36754 | GEO | 2012/09/12

SECONDARY ACCESSION(S): PRJNA156729

REPOSITORIES: GEO

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Similar Datasets

Gene expression of differentiating hESCs into otic progenitors

Project description:Stem cells, with their potential to generate different lineages, could offer a solution by replacing damaged or lost cells within the inner ear. We have shown that human embryonic stem cells can be induced to differentiate into otic progenitors, and then into hair cell-like cells and neurons that display expected electrophysiological properties. More importantly, once these otic progenitors are transplanted into animals with induced hearing loss, they differentiate and elicit a significant recovery of auditory function. The generation of otic progenitors is triggered by FGF signalling. In this dataset we have analysed the global gene expression profile of undifferentiated hESCs and compared with cultures that have been treated with FGF3 and 10, the two ligands involved in otic induction, or cultures that have been allowed to differentiate under basal conditions without FGF (DFNB). Global gene expression profiles were obtained from hESC lines H14, Shef3 and Shef1 by hybridizing samples from undifferentiated cells (Day 0) and cells exposed to either FGF3+10- or DFNB medium for 14 days. Three experimental conditions are therefore produced: hESC, FGF3+10 and DFNB.

2012-09-12 | E-GEOD-36754 | biostudies-arrayexpress

Murine Fgf3-/-;Fgf10-/- vs. Fgf3+/-;Fgf10+/- otic placode profiling

Project description:Transcriptional profiling of mouse 4-8 somite microdissected otic placodes from Fgf3/Fgf10 double heterozygotes (controls) compared to Fgf3/Fgf10 double null mutants. The purpose was to determine the effectors that are induced (or repressed) by Fgf3 and Fgf10 in the course of otic placode induction. Two condition experiment, double heterozygote vs. double null placodes. Biological replicas: 3 Fgf3+/-;Fgf10+/- and 3 Fgf3-/-;Fgf10-/- pools of ten placodes each.

2010-03-07 | E-GEOD-18702 | biostudies-arrayexpress

Murine Fgf3-/-;Fgf10-/- vs. Fgf3+/-;Fgf10+/- otic placode profiling

2010-03-01 | GSE18702 | GEO

Chick Otic Placode Induction Arrays

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

Chick Otic Placode Induction Arrays

2012-12-12 | GSE42845 | GEO

Epigenetic and transcriptomic signature reveals Sox8 as an otic master regulator

Project description:Previously FGF signalling has been shown to specify otic fate from multipotent pre-placodal ectoderm. Though many FGF target genes have been identified in subsequent studies, none of them is sufficient to induce otic lineage. Profiling and analysing the transcriptome and epigenomical signature during otic specification, we predicted and confirmed Sox8 as an otic master regulator, able to specify otic fate in the pre-placodal ectoderm. This is achieved by activating the expression of otic identity markers and compromising the fate towards lens and trigeminal ganglion. In the combat to differentiate ESCs/iPSCs or convert other cell lineage into otic lineage, our discovery may add another weaponry to tame these cells towards otic cells.

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Enhancer activation by FGF signalling during otic induction

Project description:We report that FGF exposure of sensory progenitors (pPPR) leads to rapid deposition of active chromatin marks H3K27ac near hundreds of FGF-responsive, otic-epibranchial progenitor (OEP) genes, while H3K27ac is depleted in the vicinity of non-otic genes. Genomic regions that gain H3K27ac act as cis-regulatory elements controlling OEP gene expression in time and space and define a unique transcription factor signature likely to control their activity. Thus, during ear induction FGF signalling modifies the chromatin landscape to promote enhancer activation and chromatin accessibility.

2019-09-19 | GSE137664 | GEO

Transcription profiling of mouse otic vesicle and surrounding mesenchyme and neighboring hindbrain sample from wild type and mouse mutants for FGF3, FGF10 and FGF3/FGF10 double mutants at embryonic day E10

Project description:Wild-type and mouse mutants for FGF3, FGF10 and FGF3/FGF10 double mutants at embryonic day E10 were analysed by microarrays for downregulated genes. A tissue sample corresponding to an area containing the otic vesicle and surrounding mesenchyme and neighboring hindbrain were isolated from E10 embryos (See Figure 3A of manuscript). Five samples were pooled for RNA preparation. Samples were isolated from wild-type, FGF3, FGF10 and FGF3/FGF10 double mutants. Two RNA samples for each genotype were generated (corresponding to 8 tissue samples). RNA was labeled and hybridized with Affymetrix U74A V2 arrays.

2005-09-21 | E-MEXP-430 | biostudies-arrayexpress

Enhancer activation by FGF signalling during otic induction

Project description:Enhancer activation by FGF signalling during otic induction

| PRJNA566175 | ENA

Expression data from mesodermal Tbx1-knockout otic vesicles at E11.5

Project description:The T-box transcription factor Tbx1 is expressed in the otic vesicle and surrounding periotic mesenchyme during inner ear development. Mesenchymal Tbx1 is essential for inner ear development, with conditional mutants displaying defects in both auditory and vestibular systems. We have previously identified reduced expression of retinoic acid metabolic genes in the periotic mesenchyme of mesoderm conditional Tbx1 mutants, using the T-Cre mouse line, implicating retinoic acid in mesenchymal-epithelial signaling downstream of Tbx1 in the periotic mesenchyme. In order to identify downstream effectors of mesenchymal-epithelial signaling downstream of mesenchymal Tbx1, we have utilized a gene profiling approach comparing embryonic day 11.5 otic vesicle tissue from T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and conditional heterozygous control litter mates (control). E11.5 T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and control (T-Cre conditional Tbx1 heterozygotes) embryos were microdissected to isolate the otic vesicle. Left and right ears from 3 embryos of the same genotype were pooled for each chip.

2013-01-01 | E-GEOD-34064 | biostudies-arrayexpress

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