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

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

PROVIDER: PRJNA506200 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8208930_1.fastq.gz	Fastqsanger.gz
	SRR8208930_2.fastq.gz	Fastqsanger.gz
	SRR8208931_1.fastq.gz	Fastqsanger.gz
	SRR8208931_2.fastq.gz	Fastqsanger.gz
	SRR8208932_1.fastq.gz	Fastqsanger.gz

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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

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

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

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

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

2019-05-20 | GSE127683 | GEO

In Vivo and Ex Vivo Utricles treated with ATOH1 under different promoters

Project description:Vestibular hair cells are mechanoreceptors critical for detecting head position and motion. In mammals, hair cell loss causes vestibular dysfunction as spontaneous regeneration is nearly absent. Constitutive expression of exogenous ATOH1, a hair cell transcription factor, increases regeneration of hair cells, but these cells fail to mature. With the aim of developing an optimized AAV-based ATOH1 gene therapy, we used single-cell RNA-Seq and explored the impact of defined promoters on ATOH1 transgene expression level, timing, effects in distinct cell types, and the maturity of regenerated vestibular hair cells ex vivo and in vivo.

2024-09-24 | GSE240846 | GEO

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

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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

Characterization of the transcriptomes of Atoh1-induced hair cells in the mouse cochlea

Project description:Mammalian cochlea hair cells can be regenerated from the adjacent supporting cells in many ways, however, the newly hair cells are immature and without hearing function almost. The expression of Atoh1 is an important maker of the appearance of newly hair cells, many approaches of inner ear hair cells’ regeneration are concerned with the transcription factor Atoh1. However, most new HCs are immature HCs, and they do not have the function of mature HCs and eventually die a few weeks after regeneration. Thus promoting the maturation and survival of new HCs is the primary focus of HC regeneration field. We used RNA-Seq analysis to compare the differences between the transcriptomes of Atoh1 overexpression-induced new HCs and the original HCs, and to define the factors that might help to promote the maturation and survival of new HCs.

2019-04-10 | GSE129533 | GEO

Developmental Timecourse of Mouse Utricles

2024-09-24 | GSE251853 | GEO

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

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