Identification of differentially expressed genes in early inner ear development
Ontology highlight
ABSTRACT:
ORGANISM(S): Gallus gallus
PROVIDER: GSE16918 | GEO | 2010/06/21
SECONDARY ACCESSION(S): PRJNA117713
REPOSITORIES: GEO
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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: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 vertebrate inner ear arises early in development from a thickened epithelium, the otic placode. Specification toward an otic fate requires diverse signals and complex transcriptional inputs that act sequentially and/or in parallel. To uncover and integrate novel genes with known molecular players in the gene regulatory network (GRN) underlying otic development, we have performed transcriptome analyses of the presumptive otic region at sequential early stages of commitment toward inner ear identity. Our results identify hundreds of genes enriched at specific developmental time points, revealing dynamic changes in gene expression as a function of time during the transition from progenitor to committed otic state. Initial functional analysis of selected enriched transcription factors demonstrates a genetic hierarchy amongst these genes underlying this critical transition. Our results not only characterize the otic transcriptome in unprecedented detail but also identify new links in the GRN responsible for development of the presumptive inner ear.
2017-03-09 | GSE69185 | GEO
Project description:The otic placode, from which the inner ear develops, initially forms as a thickened ectodermal patch adjacent to the dorsolateral hindbrain. Induction of otic placodal cells from human pluripotent stem cells (hPSCs) provides a robust approach to investigation of otic development. However, attempts to recapitulate otic lineage specification from hPSCs by stepwise differentiation methods have had limited success. One possible reason is that the role of signaling pathways in otic cell differentiation is not fully understood. Here, we developed a novel differentiation system involving use of suspension culture (3D floating culture) in combination with signaling factors for generating otic placodal cells via stepwise differentiation of hPSCs. We demonstrate that hPSC-derived pre-placodal cells acquired the potential to differentiate into posterior placodal cells after fibroblast growth factor 2 (FGF2) and retinoic acid (RA) treatment. Subsequent activation of WNT signaling following posterior placode specification induced differentiation of SIX1+/PAX8+/SOX2+ otic placodal cells. qPCR analysis showed that WNT activation increased expression of otocyst markers, including PAX8, PAX2, DLX5 and FBXO2. Moreover, induced otic cells exhibited similar gene expression patterns to the ventral and medial portions of the otocyst that give rise to the sensory epithelium of the inner ear. Collectively, our results indicate a critical role for FGF2, RA, and WNT signaling for the in vitro differentiation of the otic cell lineage from hPSCs. Our new culture system paves the way for improved modeling of early human inner ear development and will be of value to studies on the further differentiation of sensory epithelial cells.
2022-02-01 | GSE175998 | GEO
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.
2010-03-01 | GSE18702 | GEO
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
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:A large number of congenital hearing loss cases have an unknown genetic etiology. So far, transcriptomic approaches have successfully identified many candidate regulators of otic development, little is known about the abundance of their protein products during the development of the inner eat. Herein we used a multiplexed quantitative mass spectrometry-based proteomic approach to determine temporal trends in protein abundances during inner ear (otic) development in Xenopus. Wild type Xenopus embryos were cultured to larval stages and their otic tissues were manually dissected at five stages that represent that represent key transitions in otic morphology. The samples were processed using a bottom-up proteomic workflow and analyzed using LC-MS3.The analysis revealed dynamic expression of proteins related to cytoskeletal regulation, integrin signaling, and the extracellular matrix as inner ear structures developed. We correlated the dynamically regulated proteins in our dataset with previously published putative downstream targets of syndromic hearing loss genes SIX1 and CHD7 to identify novel candidate genes for congenital hearing loss.
2023-10-24 | PXD041991 | Pride
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