Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of organ of Corti RNA from mice carrying a null allele of Mir183 and Mir96

ABSTRACT: RNA-seq of organ of Corti RNA from mice carrying a null allele of Mir183 and Mir96

PROVIDER: PRJEB21214 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2002990_1.fastq.gz	Fastqsanger.gz
	ERR2002990_2.fastq.gz	Fastqsanger.gz
	ERR2003000_1.fastq.gz	Fastqsanger.gz
	ERR2003000_2.fastq.gz	Fastqsanger.gz
	ERR2003010_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

RNA-seq of organ of Corti RNA from mice carrying a null allele of Mir183 and Mir96

Project description:The microRNA miR-96 is important for hearing; mutations in the seed region result in dominant progressive hearing loss in mice and humans. Mir96 is expressed in the sensory hair cells of the organ of Corti along with Mir182 and Mir183. miR-96 is a master regulator of hair cell development, controlling many genes in the organ of Corti, but the role of miR-182 and miR-183 in the hair cells is unknown. We carried out RNA-seq on mice carrying a knockout allele of Mir182, and mice carrying a double knockout allele of Mir183 and Mir96 (Mir183/96). RNA was extracted from the organ of Corti from P4 homozygotes and sex-matched wildtype littermates. Strand-specific libraries were prepared using the NuGEN Ovation Mouse RNA-Seq System 1-16 kit and sequenced on an Illumina HiSeq 2500 machine as paired-end 125bp reads.

2019-03-15 | E-MTAB-5800 | biostudies-arrayexpress

RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96

Project description:Mutations affecting the microRNA miR-96 have been found to cause progressive hearing loss in humans and in mice. These initial mutations were all semidominant, so phenotypes were present in heterozygous carriers. The similarity of the phenotype between the different mutations suggested that it was the loss of normal function of Mir96 that underlay the hearing impairment. However, more recent studies of null alleles of Mir96 and the nearby Mir183, and of Mir96, Mir182 and Mir183 all together, showed that heterozygous carriers of the null alleles have no hearing phenotype, suggesting that the gain of novel targets due to the changed seed sequence resulting from point mutations is important in the Mir96 mutant phenotype, not just the loss of normal targeting. Previous transcriptome analyses of the Mir96 mutant organ of Corti showed that miR-96 controls a broad regulatory network, suggesting that a better understanding of the core genes – particularly the direct targets of miR-96 – may suggest candidate therapeutic targets. We carried out RNA-seq on mice carrying the two seed region point mutations reported in human families. RNA was extracted from the organ of Corti from four day-old homozygotes and sex-matched wildtype littermates. Strand-specific libraries were prepared following the “TruSeq Stranded mRNA Sample Preparation Guide” with the corresponding kit [Illumina Inc. Cat.# RS-122-2101 or RS-122-2102], and sequenced on an Illumina HiSeq 4000 machine as paired-end 101bp reads.

2024-02-20 | E-MTAB-13772 | biostudies-arrayexpress

RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96

2024-02-20 | E-MTAB-13772 | biostudies-arrayexpress

RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96

Project description:RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96

| PRJEB72413 | ENA

Organ of Corti size is governed by Yap/Tead-mediated progenitor self-renewal

Project description:We report on gene expression, chromatin accessibility, active histone marks distribution, and Tead DNA-binding in proliferating and postmitotic organ of Corti progenitor cells.

2020-04-24 | GSE149254 | GEO

Expression data from postnatal mouse apical and basal organ of Corti from Dicer1 conditional knockout and littermate control cochleae.

Project description:Cre recombinase-mediated conditional knockout of floxed Dicer1 alleles causes depletion of small RNAs including microRNAs, which function to repress target mRNA expression by inhibiting translation and/or stimulating mRNA degradation. We used microarrays to examine gene expression in apical versus basal organ of Corti from the cochleae of control and mutant mice in which Dicer1 was deleted and microRNAs were depleted specifically in sensory hair cells by Atoh1 promoter-driven Cre recombinase expression. Each biological replicate represents the combined apical or combined basal segments of organ of Corti from both cochleae of a single mouse. Two biological replicates for apical and basal organ of Corti from Dicer1 conditonal knockout and littermate controls were collected for RNA extraction and microarray analysis.

2012-01-01 | E-GEOD-26822 | biostudies-arrayexpress

Transcripts identified by microarray analysis that were deregulated in E18.5 Sox2(creERT2);Tbx2(fl/fl) (Sox2-Tbx2LOF) organ of Corti.

Project description:Evaluation of transcriptional changes in the E18.5 organ of Corti upon tamoxifen-induced loss of Tbx2.

2022-11-04 | GSE180501 | GEO

Pioglitazone ameliorates gentamicin ototoxicity by affecting the TLR and STAT pathways in the early postnatal organ of Corti

Project description:We evaluated the effects of pioglitazone in mouse organ of Corti (OC) explants to characterize its influence on signaling pathways involved in auditory hair cell damage. Organ of Corti explants were cultured with pioglitazone, gentamicin, or a combination of both agents. Pioglitazone treatment resulted in a significant repression of interferon (IFN)-alpha and -gamma pathways and downstream cytokines, as assessed by RNA sequencing and quantitative PCR gene expression assays. More detailed investigation at the single gene and protein level showed that pioglitazone mediated its anti-inflammatory effects through alterations of the Toll-like receptor (TLR) and STAT pathways. Together, these results indicate that pioglitazone significantly represses IFN and TLR in the cochlea, dampening the activity of gentamicin-induced pathways. These data support our previous results demonstrating significant protection of auditory hair cells in organ of Corti explants exposed to pioglitazone and other PPAR-targeted agents.

2020-09-24 | GSE158431 | GEO

The Hippo pathway and p27Kip1 cooperate to suppress sensory receptor regeneration in the organ of Corti and the retina.

Project description:The mammalian auditory sensory organ, the organ of Corti, has no capacity for regenerating lost hair cells, leading to permanent hearing impairment. In this study, we demonstrate that auditory supporting cells resist Yap activation after Hippo inhibition and uncover the molecular mechanism maintaining quiescence in the adult cochlear supporting cells.

2025-04-23 | GSE268504 | GEO

RNA-sequencing of Adult Mouse Pillar and Deiters’ Supporting Cells of the Organ of Corti

Project description:To understand the basic biological properties of supporting cells of the mammalian inner ear, we examined the transcriptome of adult pillar and Deiters’ cells. Morphologically distinct pillar and Deiters’ cells were isolated from the organ of Corti from adult CBA/J mice. One thousand pillar and Deiters’ cells were separately collected for each biological replicate, using the suction pipette technique. RNA sequencing of three biological replicates, each with two technical repeats, was performed. The resulting sequenced reads were mapped. Comparisons between pillar cells and Deiters’ cells allow identification of enriched genes, as well as differentially expressed genes that result in cellular specialization. Our dataset provides an extensive resource for understanding the molecular mechanisms underlying morphology, function, and pathology of adult mouse pillar and Deiters’ cells.

2018-08-03 | GSE111347 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data