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Single cell RNA-seq analysis of hair cell regeneration in the mammalian vestibular system and its potentiation by Atoh1

ABSTRACT: We used single cell RNA-seq to probe the transcriptional responses of utricle supporting cells to damage and Atoh1 transduction.

ORGANISM(S): Mus musculus

PROVIDER: GSE127683 | GEO | 2019/05/20

REPOSITORIES: GEO

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RNA-seq analysis of hair cell regeneration in the mammalian vestibular system and its potentiation by Atoh1

Project description:We used RNA-seq to probe the transcriptional and epigenetic responses of utricle supporting cells to damage and Atoh1 transduction.

2019-05-07 | GSE122732 | GEO

Transcriptomic and epigenetic regulation of hair cell regeneration in the mouse utricle and its potentiation by Atoh1

Project description:The mammalian cochlea loses its ability to regenerate new hair cells prior to the onset of hearing. In contrast, the adult vestibular system can produce new hair cells in response to damage, or by reprogramming of supporting cells with the hair cell transcription factor Atoh1. We used RNA-seq and ATAC-seq to probe the transcriptional and epigenetic responses of utricle supporting cells to damage and Atoh1 transduction. We show that the improved regenerative response of the utricle correlates with a more accessible chromatin structure in utricle supporting cells compared to their cochlear counterparts. We also provide evidence that Atoh1 transduction of supporting cells is able to promote increased transcriptional accessibility of some hair cell genes. Our study offers a possible explanation for regenerative differences between sensory organs of the inner ear, but shows that additional factors to Atoh1 may be required for optimal reprogramming of hair cell fate.

2019-04-30 | GSE121610 | GEO

RNA-seq analysis of hair cell regeneration in the mammalian vestibular system and its potentiation by Atoh1

Project description:RNA-seq analysis of hair cell regeneration in the mammalian vestibular system and its potentiation by Atoh1

| PRJNA506200 | ENA

Single cell RNA-seq analysis of hair cell regeneration in the mammalian vestibular system and its potentiation by Atoh1

Project description:Single cell RNA-seq analysis of hair cell regeneration in the mammalian vestibular system and its potentiation by Atoh1

| PRJNA525021 | ENA

Transcriptomic and epigenetic regulation of hair cell regeneration in the mouse utricle and its potentiation by Atoh1

Project description:Transcriptomic and epigenetic regulation of hair cell regeneration in the mouse utricle and its potentiation by Atoh1

| PRJNA497870 | ENA

Breaking the Atoh1 autoregulatory loop in hair cells: the repression of Atoh1 by Neurogenin1 during ear development

Project description:The functional unit of the inner ear consists of hair cells (HCs) and neurons in the inner ear. Both genes are induced early in development, but Atoh1 expression is counteracted by Neurog1. As a result, HC development is prevented during neurogenesis. This work aimed at understanding the molecular basis of this interaction. Atoh1 regulation depends on a 3’Atoh1-enhancer that is the site for Atoh1 autoregulation. This enhancer recapitulates Atoh1 expression in the embryo and contains putative binding sites for several transcription factors, including basic helix-loop-helix (bHLH) factors like Atoh1, Neurog1 and Hes/Hey repressors. Reporter assays on chick embryos and P19 cells show that Neurog1 hampers the autoactivation of Atoh1, the effect being cell autonomous and independent on Notch activity. ATAC-seq analysis shows that the region B of the 3’Atoh1-enhancer is accessible during development and sufficient for both activation and repression. Neurog1 requires the regions flanking the class A E-box bound by Atoh1 to show its repressor effect. However, Neurog1 does not require binding to DNA for Atoh1 repression and prevention of HC formation, but the dimerization domains Helix-1 and Helix-2. The repression of Atoh1 by Neurog1 does not involve the direct interaction between Atoh1 and Neurog1, but rather an indirect effect on the levels of Atoh1 protein. The results suggest that Neurog1 induces the acceleration of Atoh1 mRNA degradation and the consequent reduction of protein levels. Such a mechanism dissociates the prevention of Atoh1 expression in neuro-sensory progenitors from the unfolding of the neurogenic program.

2017-11-09 | GSE102649 | GEO

Atoh1 Directs Regeneration and Functional Recovery of the Mature Mouse Vestibular System.

Project description:Utricular hair cells (HCs) are mechanoreceptors required for vestibular function. After damage, regeneration of mammalian utricular HCs is limited and regenerated HCs appear immature. Thus, loss of vestibular function is presumed irreversible. Here, we found partial HC replacement and functional recovery in the mature mouse utricle, both enhanced by overexpressing the transcription factor Atoh1. Following damage, long-term fate mapping revealed that support cells non-mitotically and modestly regenerated HCs displaying no or immature bundles. By contrast, Atoh1 overexpression stimulated proliferation and widespread regeneration of HCs exhibiting elongated bundles, patent mechanotransduction channels, and synaptic connections. Finally, although damage without Atoh1 overexpression failed to initiate or sustain a spontaneous functional recovery, Atoh1 overexpression significantly enhanced both the degree and percentage of animals exhibiting sustained functional recovery. Therefore, the mature, damaged utricle has an Atoh1-responsive regenerative program leading to functional recovery, underscoring the potential of a reprogramming approach to sensory regeneration.

| S-EPMC6659123 | biostudies-literature

Transcriptomic and epigenetic regulation of hair cell regeneration in the mouse utricle and its potentiation by Atoh1.

Project description:The mammalian cochlea loses its ability to regenerate new hair cells prior to the onset of hearing. In contrast, the adult vestibular system can produce new hair cells in response to damage, or by reprogramming of supporting cells with the hair cell transcription factor Atoh1. We used RNA-seq and ATAC-seq to probe the transcriptional and epigenetic responses of utricle supporting cells to damage and Atoh1 transduction. We show that the regenerative response of the utricle correlates with a more accessible chromatin structure in utricle supporting cells compared to their cochlear counterparts. We also provide evidence that Atoh1 transduction of supporting cells is able to promote increased transcriptional accessibility of some hair cell genes. Our study offers a possible explanation for regenerative differences between sensory organs of the inner ear, but shows that additional factors to Atoh1 may be required for optimal reprogramming of hair cell fate.

| S-EPMC6504235 | biostudies-literature

Regenerating hair cells in human vestibular sensory epithelia

Project description:To investigate alterations in gene expression after Ad2-ATOH1-GFP transduction of human supporting cells, we measured transcriptome changes by RNA-seq. We compared gentamicin-treated tissue (to kill the hair cells) transduced with Ad2-ATOH1-GFP (to promote hair cell production) cultured for 5 days, versus control tissues only treated with gentamicin (cultured for 2 days, 8 days and 14-18 days).

2018-07-16 | GSE109320 | GEO

Three distinct Atoh1 enhancers cooperate for sound receptor hair cell development [ATAC-seq]

Project description:Cochlear hair cells (HCs) in the inner ear are responsible for sound detection. For HC fate specification, the master transcription factor Atoh1 is both necessary and sufficient. Atoh1 expression is dynamic and tightly regulated during development, but the cis-regulatory elements mediating this regulation remain unresolved. Unexpectedly, we found that deleting the only recognized Atoh1 enhancer, defined here as Eh1, failed to impair HC development. By using ATAC-seq (assay for transposase-accessible chromatin with high-throughput sequencing), we discovered two additional Atoh1 enhancers: Eh2 and Eh3. Notably, Eh2 deletion was sufficient for impairing HC development, and concurrent deletion of Eh1 and Eh2 or all three enhancers resulted in nearly complete absence of HCs. Lastly, we showed that Atoh1 binds to all three enhancers, consistent with its autoregulatory function. Our findings reveal that the cooperative action of three distinct enhancers underpins effective Atoh1 regulation during HC development, indicating potential therapeutic approaches for HC regeneration.

2022-07-22 | GSE181310 | GEO

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