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Loss of Mst1/2 activity promotes non-mitotic hair cell generation in the neonatal organ of Corti

ABSTRACT: Loss of Mst1/2 activity promotes non-mitotic hair cell generation in the neonatal organ of Corti

PROVIDER: PRJNA882443 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21641039_1.fastq.gz	Fastqsanger.gz
	SRR21641039_2.fastq.gz	Fastqsanger.gz
	SRR21641040_1.fastq.gz	Fastqsanger.gz
	SRR21641040_2.fastq.gz	Fastqsanger.gz
	SRR21641041_1.fastq.gz	Fastqsanger.gz

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Loss of Mst1/2 activity promotes non-mitotic hair cell generation in the neonatal organ of Corti

Project description:We used in vitro RNA-sequencing to show that the Hippo signaling pathway is involved in HC damage and self-repair processes. Turning off Hippo signaling through Mst1/2 inhibition or Yap overexpression induces YAP nuclear accumulation, especially in supporting cells, which induces supernumerary HC production and HC regeneration after injury. Mechanistically, these effects of Hippo signaling work synergistically with the Notch pathway.

2022-09-25 | GSE213784 | GEO

RNA-sequencing of Adult Mouse Inner Hair Cells and Outer Hair Cells of the organ of Corti

Project description:To further understand the biological properties of hair cells of the mammalian cochlea, we examined the transcriptome of adult inner and outer hair cells. Morphologically distinct inner and outer hair cells were isolated from the organ of Corti from adult CBA/J mice. One thousand inner and outer hair cells were separately collected for each biological replicate, using the suction pipette technique. RNA sequencing of two biological replicates of IHCs and three biological replicates of OHCs, each with two technical repeats, was performed. The resulting sequenced reads were mapped. Comparisons between inner and outer hair 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 inner and outer hair cells.

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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

PROX1 Controls Cellular Patterning, Innervation and Differentiation in the Mouse Organ of Corti

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

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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

Loss of Mst1/2 activity promotes non-mitotic hair cell generation in the neonatal organ of Corti.

Project description:Mammalian sensory hair cells (HCs) have limited capacity for regeneration, which leads to permanent hearing loss after HC death. Here, we used in vitro RNA-sequencing to show that the Hippo signaling pathway is involved in HC damage and self-repair processes. Turning off Hippo signaling through Mst1/2 inhibition or Yap overexpression induces YAP nuclear accumulation, especially in supporting cells, which induces supernumerary HC production and HC regeneration after injury. Mechanistically, these effects of Hippo signaling work synergistically with the Notch pathway. Importantly, the supernumerary HCs not only express HC markers, but also have cilia structures that are able to form neural connections to auditory regions in vivo. Taken together, regulating Hippo suggests new strategies for promoting cochlear supporting cell proliferation, HC regeneration, and reconnection with neurons in mammals.

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Epigenetic analysis of perinatal maturation of supporting cells in the organ of Corti

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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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.

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RNA-sequencing of Adult Mouse Inner Hair Cells and Outer Hair Cells of the organ of Corti

Project description:RNA-sequencing of Adult Mouse Inner Hair Cells and Outer Hair Cells of the organ of Corti

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