Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomes of control and Chd7-deficient spiral ganglia neurons and cochlear hair cells

ABSTRACT: Transcriptomes of control and Chd7-deficient spiral ganglia neurons and cochlear hair cells

PROVIDER: PRJNA687552 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13298207_1.fastq.gz	Fastqsanger.gz
	SRR13298207_2.fastq.gz	Fastqsanger.gz
	SRR13298208_1.fastq.gz	Fastqsanger.gz
	SRR13298208_2.fastq.gz	Fastqsanger.gz
	SRR13298209_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Transcriptomes of control and Chd7-deficient spiral ganglia neurons and cochlear hair cells

Project description:The aim of this study is to identify the gene targets of Chd7 (by RNA-seq) in spiral ganglia neurons and cochlear hair cells. mRNA profiles of FACS-sorted spiral ganglia neurons from 4-day old mice and cochlear hair cells from embryos af 16.5 days in controls, Chd7 heterozygous and Chd7 homozygous mutant animals were generated by paired-end sequencing, in triplicate, using Illumina HiSeq 4000. The sequence reads that passed quality filters were reads were aligned to mouse MM10 genome assembly using HiSAT2 (version 2.1.0) with the default parameters in Galaxy (version 2.1.0). To facilitate quantitative gene expression analysis, aligned reads for each sample were counted using featureCounts (version1.6.4). Differential gene expression analysis was performed using DESeq2 (version 2.11.40.6), applying parametric fit. qRT–PCR validation was performed using SYBR Green and gene specific primers. To identify differentially expressed genes, RPKM values of genes that are not normally expressed in E16.5 hair cells or P4 spiral ganglia neurons were removed from analysis. This resulted in 6910 transcripts for genes expressed in hair cells and 11293 genes expressed in neurons. A pairwise comparison between controls and homozygotes and controls and heterozygotes was performed. Significant thresholds were considered for transcripts with an adjusted p-value (FDR) of ≤0.05 and linear fold change of >2 in either direction. Altered expression of selected genes was confirmed with qRT–PCR as well as the encoded proteins by immunohistochemistry. Analysis of differentially expressed genes uncovered novel targets and potential mechanisms by which Chd7 controls the survival of these cells during normal hearing.

2021-11-10 | GSE163798 | GEO

Profiling mouse cochlear cell maturation using 10X Genomics single-cell transcriptomics

Project description:Juvenile and mature mouse cochleae contain various low-abundant, vulnerable sensory epithelial cells embedded in the calcified temporal bone, making it challenging to profile the dynamic transcriptome changes of these cells during maturation at the single-cell level. Here we performed the 10X Genomics single-cell RNA sequencing (scRNA-seq) of mouse cochleae at postnatal days 14 (P14) and 28. We attained the transcriptomes of multiple cell types, including hair cells, supporting cells, spiral ganglia, stria fibrocytes, and immune cells. Our hair cell datasets are consistent with published transcripts from bulk RNA seq and scRNA-seq. We also mapped known deafness genes to corresponding cochlear cell types. Importantly, pseudotime trajectory analysis revealed that inner hair cells peak their maturation at P14 while outer hair cells continue to develop until P28. We further identified and confirmed a long noncoding RNA gene Miat expressed during maturation in cochlear hair cells and spiral ganglia neurons. Our transcriptomes of juvenile and mature mouse cochlear cells provided the sequel to those previously published at late embryonic and early postnatal ages and will be valuable resources to investigate cochlear maturation at single-cell resolution.

2022-08-19 | GSE202920 | GEO

RNA-seq analysis of neonatal mouse cochlear hair cells

Project description:This study examined transcripts that are enriched in neonatal mouse cochlear hair cells. Hair cells were purified by FACS sorting for GFP fluorescence from the cochleas of transgenic mice in which the endogenous Atoh1 gene was fused with GFP Two replicates of GFP+ hair cells were compared with all other cochlear cell types that were GFP-

2015-03-01 | E-GEOD-65633 | biostudies-arrayexpress

The upregulation of K+ and HCN channels in developing spiral ganglion neurons is mediated by cochlear inner hair cells

Project description:Spiral ganglion neurons (SGNs) are primary sensory afferent neurons that relay acoustic information from the cochlear inner hair cells (IHCs) to the brainstem. The response properties of different SGNs diverge to represent a wide range of sound intensities in an action-potential code. This biophysical heterogeneity is established during pre-hearing stages of development, a time when IHCs fire spontaneous Ca2+ action potentials that drive glutamate release from their ribbon synapses onto the SGN terminals. The role of spontaneous IHC activity in the refinement of SGN characteristics is still largely unknown. Using pre-hearing otoferlin knockout mice (Otof-/-), in which Ca2+-dependent exocytosis in IHCs is abolished, we found that developing SGNs fail to upregulate low-voltage-activated K+-channels and hyperpolarisation-activated cyclic-nucleotide-gated channels. This delayed maturation resulted in hyperexcitable SGNs with immature firing characteristics. We have also shown that SGNs that synapse with the pillar side of the IHCs selectively express a resurgent K+ current, highlighting a novel biophysical marker for these neurons. RNA-sequencing showed that several K+ channels are downregulated in Otof-/- mice, further supporting the electrophysiological recordings. Our data demonstrate that spontaneous Ca2+-dependent activity in pre-hearing IHCs regulates some of the key biophysical and molecular features of the developing SGNs. KEY POINTS: Ca2+-dependent exocytosis in inner hair cells (IHCs) is otoferlin-dependent as early as postnatal day 1. A lack of otoferlin in IHCs affects potassium channel expression in SGNs. The absence of otoferlin is associated with SGN hyperexcitability. We propose that type I spiral ganglion neuron functional maturation depends on IHC exocytosis.

2024-09-27 | GSE242669 | GEO

Comprehensive transcriptome analysis of cochlear spiral ganglion neurons at multiple ages

Project description:Inner ear cochlear spiral ganglion neurons (SGNs) transmit sound information to the brainstem. Recent single cell RNA-Seq studies have revealed heterogeneities within SGNs. Nonetheless, much remains unknown about the transcriptome of SGNs, especially which genes are specifically expressed in SGNs. To address these questions, we needed a deeper and broader gene coverage than that in previous studies. We performed bulk RNA-Seq on mouse SGNs at five ages, and on two reference cell types (hair cells and glia). Their transcriptome comparison identified genes previously unknown to be specifically expressed in SGNs. To validate our dataset and provide useful genetic tools for this research field, we generated two knockin mouse strains: Scrt2-P2A-tdTomato and Celf4-3xHA-P2A-iCreER-T2A-EGFP. Our comprehensive analysis confirmed the SGN-selective expression of the candidate genes, testifying to the quality of our transcriptome data. These two mouse strains can be used to temporally label SGNs or to sort them.

2020-01-07 | GSE132925 | GEO

RNA-seq analysis of neonatal mouse cochlear hair cells

2015-03-01 | GSE65633 | GEO

The upregulation of K+ and HCN channels in developing spiral ganglion neurons is mediated by cochlear inner hair cells

Project description:The upregulation of K+ and HCN channels in developing spiral ganglion neurons is mediated by cochlear inner hair cells

| PRJNA1013999 | ENA

Unraveling the Molecular Landscape of Lead-Induced Cochlear Synaptopathy: A Quantitative Proteomic Analysis

Project description:This study investigates how lead exposure triggers cochlear synaptopathy and hearing loss in mice. Young-adult CBA/J mice were given lead acetate in drinking water for 28 days. We assessed hearing thresholds, outer hair cell activity, and synaptic changes in the cochlea. Lead exposure raises hearing thresholds, indicating cochlear synaptopathy. Notably affects synapses in the basal turn without impacting outer hair cells. In addition to this, lead altered the abundance of 352 synaptic proteins, with the synaptic vesicle cycle pathway prominently affected. Lead-induced cochlear synaptopathy targets basal cochlear regions, implicating synaptic vesicle cycle signaling in hearing loss. Revealing specific mechanisms behind lead-induced hearing deficits enhances targeted interventions and preventive strategies, advancing our understanding of lead induced hearing loss.

2024-10-17 | PXD050415 | Pride

Transcriptional profiling of cochlear spiral ganglion neurons and lateral wall cells

Project description:Transcriptional profiling of cochlear spiral ganglion neurons and lateral wall cells

| PRJNA705914 | ENA

Comprehensive transcriptome analysis of cochlear spiral ganglion neurons at multiple ages

Project description:Comprehensive transcriptome analysis of cochlear spiral ganglion neurons at multiple ages

| PRJNA549471 | ENA