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

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

PROVIDER: PRJNA627734 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11601247_1.fastq.gz	Fastqsanger.gz
	SRR11601247_2.fastq.gz	Fastqsanger.gz
	SRR11601248_1.fastq.gz	Fastqsanger.gz
	SRR11601248_2.fastq.gz	Fastqsanger.gz
	SRR11601249_1.fastq.gz	Fastqsanger.gz

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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

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

Project description:Precise control of organ growth and patterning is executed through a balanced regulation of progenitor self-renewal and differentiation. In the auditory sensory epithelium-the organ of Corti-progenitor cells exit the cell cycle in a coordinated wave between E12.5 and E14.5 before the initiation of sensory receptor cell differentiation, making it a unique system for studying the molecular mechanisms controlling the switch between proliferation and differentiation. Here we identify the Yap/Tead complex as a key regulator of the self-renewal gene network in organ of Corti progenitor cells. We show that Tead transcription factors bind directly to the putative regulatory elements of many stemness- and cell cycle-related genes. We also show that the Tead coactivator protein, Yap, is degraded specifically in the Sox2-positive domain of the cochlear duct, resulting in down-regulation of Tead gene targets. Further, conditional loss of the Yap gene in the inner ear results in the formation of significantly smaller auditory and vestibular sensory epithelia, while conditional overexpression of a constitutively active version of Yap, Yap5SA, is sufficient to prevent cell cycle exit and to prolong sensory tissue growth. We also show that viral gene delivery of Yap5SA in the postnatal inner ear sensory epithelia in vivo drives cell cycle reentry after hair cell loss. Taken together, these data highlight the key role of the Yap/Tead transcription factor complex in maintaining inner ear progenitors during development, and suggest new strategies to induce sensory cell regeneration.

| S-EPMC7306825 | biostudies-literature

Mesocestoides corti

Project description:Mesocestoides corti overview

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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

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

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Project description:Mesocestoides corti Raw sequence reads

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Mesocestoides corti

Project description:Mesocestoides corti Raw sequence reads

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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

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.

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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

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