Ontology highlight
ABSTRACT:
PROVIDER: PRJNA967984 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24457585_1.fastq.gz | Fastqsanger.gz | |||
| SRR24457585_2.fastq.gz | Fastqsanger.gz | |||
| SRR24457586_1.fastq.gz | Fastqsanger.gz | |||
| SRR24457586_2.fastq.gz | Fastqsanger.gz | |||
| SRR24457587_1.fastq.gz | Fastqsanger.gz |
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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:* Bone signaling in middle ear development * <br/>Common middle ear diseases, such as chronic suppurative otitis media and cholesteatoma, may affect bone behavior in the middle ear air cell system. <br/> This study analyzed gene expression of bone-related signaling factors and gene sets from lining tissues in the developing middle ear of the rat. Candidate gene products were compared with previously published data on middle ear bone metabolism. <br/> Microarray technology was used to identify bone-related genes and gene sets, which were differentially expressed between the adult (quiescent) bulla and young (resorbing/forming) bulla. <br/><br/> * Gene expression of the otic capsule *<br/>The behavior of bone cells within the otic capsule is unique. After occification localized bone remodeling is virtually absent. Human otosclerosis is a localized disease within the otic capsule where the bone starts to remodel pathologically. Disease etiology is unknown and the pathogenesis is only partially elucidated.<br/><br/> The objective of this study is to measure bone-related gene expression of the otic capsule in order to reveal additionally signaling factors responsible for the absent bone remodeling within the otic capsule.<br/><br/> Microarray technology was used to determine genes involved in the bone metabolism, which were differentially expressed between lining tissues from the otic capsule and lining tissues from the middle ear of the rat.
2014-02-20 | E-MTAB-2336 | biostudies-arrayexpress
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:Mutations in the chromatin remodeling enzyme CHD7 cause CHARGE syndrome, which affects multiple organs including the inner ear. We investigated how CHD7 mutations affect otic development in human inner ear organoids. We found loss of CHD7 or its chromatin remodeling activity leads to complete absence of hair cells and supporting cells, which can be explained by dysregulation of key otic development-associated genes in mutant otic progenitors. Further analysis of the mutant otic progenitors suggested that CHD7 can regulate otic genes through a chromatin remodeling-independent mechanism. Results from transcriptome profiling of hair cells revealed disruption of deafness gene expression as a potential underlying mechanism of CHARGE-associated sensorineural hearing loss. Notably, co-differentiating CHD7 knockout and wild-type cells in chimeric organoids partially rescued mutant phenotypes by restoring otherwise severely dysregulated otic genes. Taken together, our results suggest that CHD7 plays a critical role in regulating human otic lineage differentiation and deafness gene expression.
2022-07-21 | GSE208585 | GEO
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.
2022-08-01 | GSE102825 | GEO
Project description:Inner ear morphogenesis requires tightly regulated epigenetic and transcriptional control of gene expression. CHD7, an ATP-dependent chromodomain helicase DNA-binding protein, and SOX2, an SRY-related HMG box pioneer transcription factor, are known to contribute to vestibular and auditory system development, but their genetic interactions in the ear have not been explored. Here, we analyzed inner ear development and the transcriptional regulatory landscapes in mice with variable dosage of Chd7 and/or Sox2. We show that combined haploinsufficiency for Chd7 and Sox2 results in reduced otic cell proliferation, severe malformations of semicircular canals, and shortened cochlea with ectopic hair cells. Examination of mice with conditional, inducible Chd7 loss by Sox2CreER reveals a critical period (~E9.5) of susceptibility in the inner ear to combined Chd7 and Sox2 loss. Data from genome-wide RNA-sequencing and CUT&Tag studies in the otocyst show that CHD7 regulates Sox2 expression and acts early in a gene regulatory network to control expression of key otic patterning genes, including Pax2 and Otx2. CHD7 and SOX2 directly bind independently and cooperatively at transcription start sites and enhancers to regulate otic progenitor cell proliferation and function. Together, our findings reveal essential roles for Chd7 and Sox2 in the early inner ear and may be applicable for CHD7 and SOX2 related syndromic and other forms of hearing or balance disorders.
2024-03-01 | GSE239362 | 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: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:An abundance of research has recently highlighted the susceptibility of cochleovestibular ganglion (CVG) neurons to noise damage and aging in the adult cochlea, resulting in hearing deficits. Furthering our understanding of the transcriptional cascades that contribute to CVG development may provide insight into how these cells can be regenerated to treat inner ear dysfunction. Here we perform a high-depth single-cell RNA sequencing analysis of the E10.5 otic vesicle and its surrounding tissues, including CVG precursor neuroblasts and emerging CVG neurons. Clustering and trajectory analysis of otic lineage cells reveals otic markers and the changes in gene expression that occur from neuroblast delamination towards the development of the CVG. This dataset provides a valuable resource for further identifying the mechanisms associated with CVG development from neurosensory competent cells within the otic vesicle.
2023-05-02 | GSE231513 | GEO
Project description:The first morphological evidence of the developing ear is a thickened disk of ectoderm known as the otic placode. However, signals for otogenesis are present even before the otic placode is physically apparent. Several inductive signals have been identified through candidate gene approaches, but there are still many gaps in the signaling cascade of otogenesis. Presently the candidate gene approach has largely exhausted known candidates. This project compares the pre-otic domain with a control region that is competent, but not specified to form otic placode. The purpose of this work is to identify genes that are differentially expressed in the pre-otic domain in order to generate a list of novel candidate genes for otic placode induction.
2010-06-21 | GSE16918 | GEO