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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Morag Lewis

PROVIDER: E-MTAB-5800 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

Analysis of RNA associated with the RISC complex (Ago2) in four day old mice carrying a mutation in miR-96

Project description:The diminuendo mouse carries a mutation in the seed region of miR-96. Homozygotes are deaf and exhibit vestibular dysfunction, heterozygotes display rapidly progressive hearing loss. Some targets of miR-96 are known, but it is likely that many still remain to be discovered. MicroRNAs function by recruiting the RISC complex to their mRNA targets, so one way to examine the mRNAs being controlled by microRNAs in a cell is to immunoprecipitate Ago2, one of the RISC proteins, and extract the RNA bound to it. This should detect all the mRNAs being targetted by microRNAs in the tissue. We extracted mRNA bound to Ago2 from the organs of Corti and olfactory bulbs of diminuendo homozygote and wildtype littermates at four days old, and carried out microarray analysis.

2016-02-26 | E-MTAB-3737 | biostudies-arrayexpress

Expression of Atoh1, Gfi1, and Pou4f3 in the mature cochlea reprograms non-sensory cells into hair cells

Project description:Mechanosensory hair cells of the mature mammalian organ of Corti do not regenerate, and loss of hair cells leads to permanent hearing loss. Although non-mammalian vertebrates are able to regenerate hair cells by the division and transdifferentiation of adjacent supporting cells, many humans with severe hearing loss completely lack hair cells and supporting cells, with the organ of Corti being replaced by a flat epithelium of non-sensory cells To determine if mature non-sensory cells can produce hair cells in vivo, we reprogrammed non-sensory cells of the mature cochlea with three hair cell transcription factors, Gfi1, Atoh1, and Pou4f3. We were able to generate significant numbers of hair cell-like cells in the non-sensory inner and outer sulci of the cochlea after 2 weeks of reprogramming. New hair cells continued to be added to the non-sensory regions of the cochlea over the next seven weeks, and expressed hair cell proteins such as Myosin VIIa, parvalbumin, and prestin and formed stereociliary hair bundles. We confirmed the identity of these cells by high depth single cell RNA-seq. Significantly, cells adjacent to converted hair cells expressed markers of supporting cells, suggesting that transcription factor reprogramming of non-sensory tissue in the adult animal can generate mosaics of sensory cells similar to those seen in the organ of Corti. Generating such sensory mosaics by reprogramming may represent a potential strategy for hearing restoration in humans.

2024-01-03 | GSE224627 | GEO

RNA-seq of inner ear RNA from mice carrying a mutation in Zfp719 and wildtype controls at 3 different ages

Project description:The function of zinc finger protein 719 (Zfp719) remains largely unknown. The most closely related human gene ZNF175 encodes protein OTK18 which has 44% amino acid identity with mouse Zfp719, and is thought to be a transcriptional suppressor. Zfp719-deficient mice showed highly elevated auditory brainstem response (ABR) thresholds at 14 weeks in a high-throughput targeted mutagenesis programme (the Wellcome Trust Sanger Institute’s Mouse Genetics Project). In order to understand the regulatory changes caused by the reduction in Zfp719, we carried out RNA-seq on RNA extracted from the inner ears of wildtypes and sex-matched homozygotes at three different ages; four days, two weeks and three weeks old, to look at expression before maturation of the auditory system, and before and after the onset of hearing loss. Strand-specific libraries were prepared using TruSeq stranded mRNA LT kit and sequenced on an Illumina NextSeq 500 machine as paired-end 150bp reads.

2023-12-01 | E-MTAB-7414 | biostudies-arrayexpress

Microarray analysis of newborn mice carrying a mutation in miR-96, compared to wildtype sex-matched littermate controls.

Project description:The diminuendo mouse carries a mutation in the seed region of miR-96. Adult homozygotes are deaf and display vestibular defects, heterozygotes have rapidly progressive hearing loss. Microarray analysis of four day old homozygotes showed multiple transcripts were misregulated. Because the effect of the diminuendo mutation appears to be a retardation of development, we carried out this microarray on newborn homozygote and wildtype mice to examine the transcriptome at a younger age.

2016-02-26 | E-MTAB-3735 | biostudies-arrayexpress

scRNA-seq of P2 mouse cochlea

Project description:Purpose and Methods: Cochlear sensory hair cells (HCs) are essential for our sense of hearing. They are embedded in the organ of Corti that lacks regenerative capacity, which is a major cause of hearing loss. However, some neonatal non-sensory cells in the organ of Corti display a limited regenerative ability. We used fluorescence-activated cell sorting (FACS) to isolate different cochlear cell types from postnatal day 2 (P2) mice to assess the individual cell groups’ potential to grow organoids and to generate new HCs. Single-cell RNAseq validated the composition of the cell types in the sorted cell groups. Results and Conclusions: The greater epithelial ridge (GER), a transient tissue that only exists in the neonatal inner ear, harbored the most potent organoid-forming cells. GER-derived organoids expanded into large colonies when cultured adherently and gave rise to new hair cell marker-expressing cells in a sensory epithelia-resembling organization. The organoid forming ability of GER cells was synergistically enhanced when they were cultured at increasing density. The synergistic effect relied on direct cell-to-cell contact rather than released soluble factors.

2020-12-29 | GSE162308 | GEO

Hypervulnerability to sound-exposure through impaired adaptive proliferation of peroxisomes

Project description:A deficiency of pejvakin, a protein of unknown function, causes a strikingly heterogeneous form of deafness. Pejvakin-deficient (Pjvk-/-) mice also exhibited variable auditory phenotypes. Correlation between their hearing thresholds and the number of pups per cage suggested a possible harmful effect of pup vocalizations. Direct sound or electrical stimulation showed that the cochlear sensory hair cells and auditory pathway neurons of Pjvk-/- mice and patients were exceptionally vulnerable to sound. Pjvk-/- cochleas displayed features of marked oxidative stress and impaired anti-oxidant defenses. We showed that pejvakin is associated with peroxisomes, and is required for the oxidative stress-induced proliferation of these organelles. In Pjvk-/- hair cells, peroxisomes displayed structural abnormalities after the onset of hearing. Noise-exposure of wild-type mice rapidly upregulated Pjvk cochlear transcription, and triggered peroxisome proliferation in hair cells and primary auditory neurons. Our results reveal that the anti-oxidant activity of peroxisomes protects the auditory system against noise-induced damage. Three RNA samples was extracted from dissected organ of Corti (OC) for each genotype (Pjvk-/- and Pjvk+/+ mice) and analyzed (triplicate OCmm-1, OCmm-2, and OCmm-3 for Pjvk-/-, and triplicate OCpp-1, OCpp-2, and OCpp-3 for Pjvk+/+).

2015-12-31 | E-GEOD-72722 | biostudies-arrayexpress

Transcription profiling of mouse mutant for microRNA-96 vs. wildtype mice to identify potential targets

Project description:The Diminuendo mouse mutant strain displays progressive deafness and carries a mutation in the gene mmu-mir-96, a microRNA. We carried out a microarray analysis using RNA extracted from the organ of Corti from 4-day old mutant (n=6) and wildtype (n=6) mice to compare gene expression of both direct and indirect targets.

2009-03-26 | E-TABM-489 | biostudies-arrayexpress

MicroRNAs Involved in Aging of the Lateral Wall of the Cochlear Duct

Project description:Age-related hearing loss is a progressive sensorineural hearing loss that occurs as people get older. Degeneration of the organ of Corti and atrophy of the lateral wall of the cochlear duct (or scala media) in the inner ear are the two primary causes. MicroRNAs (miRNAs), a class of short non-coding RNAs that regulate the expression of mRNA/protein targets, are important regulators of cellular senescence and aging. We examined the change of miRNA gene expression profiles in the lateral wall of the cochlear duct in two mouse strains during aging The totoal RNA was extracted from the lateral wall of cochlear duct from CBA/J and C57BL/6J mice at different ages. The expression profile of miRNAs was examined by miR microarray GeneChip.

2014-10-01 | E-GEOD-57782 | biostudies-arrayexpress

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