RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96
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ABSTRACT:
PROVIDER: PRJEB72413 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12645100_1.fastq.gz | Fastqsanger.gz | |||
| ERR12645100_2.fastq.gz | Fastqsanger.gz | |||
| ERR12645101_1.fastq.gz | Fastqsanger.gz | |||
| ERR12645101_2.fastq.gz | Fastqsanger.gz | |||
| ERR12645102_1.fastq.gz | Fastqsanger.gz |
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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
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
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.
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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.
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Project description:The organ of Corti is divided into functional compartments responsible for hearing or cochlear amplification. A medial compartment containing inner hair cells innervated by Type I spiral ganglion neurons and a lateral compartment containing outer hair cells innervated by Type II spiral ganglion neurons. Supporting cells also differ, with lateral compartment pillar cells and Deiters’ cells developing specialized cellular structures to support outer hair cell electromotility. We bred organ of Corti-restricted Prox1 conditional knockout mice to study lateral compartment development because PROX1 is the first transcription factor expressed strictly in lateral compartment supporting cells. In the absence of Prox1, supporting cell numbers increased without corresponding changes in outer hair cells, and they appear incompletely differentiated based on morphological criteria. Outer hair cell number was not impacted but innervation was disrupted with many afferent neurons turning incorrectly towards the cochlear apex. RNAseq revealed no changes in gene expression that could account for the innervation phenotype. Therefore, we propose that PROX1 promotes pillar and Deiters’ cell differentiation and organization that has secondary effects on innervation but is not required for compartment specification.
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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
Project description:RNA-seq of organ of Corti RNA from mice carrying a null allele of Mir183 and Mir96
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Project description:Evaluation of transcriptional changes in the E18.5 organ of Corti upon tamoxifen-induced loss of Tbx2.
2022-11-04 | GSE180501 | GEO
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
Project description:Sensory hair cells cannot be regenerated through transdifferentiation of neighboring supporting cells in the organ of Corti in mature mammalian animals, but limited regeneration capacity exists in supporting cells at neonatal stage in mouse and this transdifferentiation potential is rapidly lost during the first week of postnatal maturtion. We hypothesized that epigenetic decommissioning of hair cell gene enhancers in supporting cells during postnatal maturation leads the permanent silencing of hair cell genes and the loss of transdifferentiation potential. To test this hypothesis, we FACS purified hair cells and supporting cells from cochleae at different developmental stages for transcritomic analysis (RNAseq), chromatin accessibility assay (ATACseq) and histone modification profiling (ChIPseq or CUT&RUN). We first defined hair cell genes and predicted their potential active enhancers. We found that hair cell gene promoters and enhancers were kept in a primed-but-silenced status (H3K4me1/3+, low H3K27ac but high H3K27me3) in supporting cells at neonatal stage. During postnatal maturation, hair cell gene enhancers are decommissioned through H3K4me1 removal, leading to the permanent silencing of hair cells genes. We also found that hair cell gene enhancer decommissioning process correlated with the base-to-apex wave of transdifferentiation potential loss. In addition, hair cell gene enhancer commissioning status is preserved in mature utricular supporting cells, which can regenerate hair cells through transdifferentiation even at adult stage. Those data together suggest that decommissioning of hair cell gene enhancers in supporting cells during postnatal maturation is the epigenetic mechanism underlying the loss of regeneration capacity in the organ of Corti.
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