Murine Fgf3-/-;Fgf10-/- vs. Fgf3+/-;Fgf10+/- otic placode profiling
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE18702 | GEO | 2010/03/01
SECONDARY ACCESSION(S): PRJNA121491
REPOSITORIES: GEO
Similar Datasets
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: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
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:Murine Fgf3-/- Fgf10-/- vs. Fgf3+/- Fgf10+/- otic placode profiling
| PRJNA121491 | ENA
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
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).
2012-09-12 | GSE36754 | GEO
Project description:We performed this experiment to identify the primary target of Fgf10 in lung development. We used a double transgenic system to either attenuate FGFR2b ligands Rosa26rtTAtet(O)solubleR2b based on the use of doxycycline we generated the samples after 6 and 9 hours of doxycyline induction, or to increase Fgf10 using Rosa26rtTAtet(O)fgf10 double transgenic system we generated samples after 9 of doxycycline induction, controls lungs are provided
2019-01-25 | GSE124154 | GEO
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. 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