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Effects of Nogo-A deletion in the dental epithelium of the continuously growing mouse incisor

ABSTRACT: Effects of Nogo-A deletion in the dental epithelium of the continuously growing mouse incisor

PROVIDER: PRJNA674603 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12979859.fastq.gz	Fastqsanger.gz
	SRR12979860.fastq.gz	Fastqsanger.gz
	SRR12979861.fastq.gz	Fastqsanger.gz
	SRR12979862.fastq.gz	Fastqsanger.gz
	SRR12979863.fastq.gz	Fastqsanger.gz

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Effects of Nogo-A deletion in the dental epithelium of the continuously growing mouse incisor

Project description:Nogo-A is a major player in the regulation of neural development and regeneration, and it is the target of several clinical trials. Despite its high clinical relevance, the functions of Nogo-A outside the central nervous system are mostly unknown. In this work, we investigated the role of Nogo-A in tooth development in mouse transgenic models. We observed that Nogo-A is expressed in ameloblasts, the cells responsible for the formation of enamel. We show that the deletion of Nogo-A in the dental epithelium leads to the formation of defective enamel. By RNA sequencing we showed that this phenotype is associated with the overexpression of clusters of genes involved in cell differentiation and production of enamel.

2022-01-01 | GSE160829 | GEO

Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Microarray Expression]

Project description:Regulation of transit amplifying cell formation from self-renewing stem cell is fundamental process for cell replacement in a controlled way. Here we analyse the properties of a population of mesenchymal TACs in the continuously growing mouse incisor to identify key components of the molecular regulation that drives proliferation. Using gene microarray profiling, we show that the polycomb repressive complex 1 acts as a global regulator of the TAC phenotype by its direct action on the expression of key cell cycle regulatory genes and also by regulating Wnt/b-catenin signalling activity. Analysing the properties of mesenchymal transit amplifying cells population and identifing key components of the molecular regulation that drives proliferation.

2019-03-12 | GSE104934 | GEO

Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Ring1b ChIP]

Project description:Regulation of transit amplifying cell formation from self-renewing stem cell is fundamental process for cell replacement in a controlled way. Here we analyse the properties of a population of mesenchymal TACs in the continuously growing mouse incisor to identify key components of the molecular regulation that drives proliferation. We show that the polycomb repressive complex 1 acts as a global regulator of the TAC phenotype by its direct action on the expression of key cell cycle regulatory genes and also by regulating Wnt/b-catenin signalling activity. We also identify an essential requirement for TACs in maintaining the mesenchymal stem cells, indicative of a positive feedback mechanism. Analysing the properties of mesenchymal transit amplifying cells population and identifing key components of the molecular regulation that drives proliferation.

2019-03-12 | GSE104892 | GEO

Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Histone ChIP]

Project description:Regulation of transit amplifying cell formation from self-renewing stem cell is fundamental process for cell replacement in a controlled way. Here we analyse the properties of a population of mesenchymal TACs in the continuously growing mouse incisor to identify key components of the molecular regulation that drives proliferation. We show that the polycomb repressive complex 1 acts as a global regulator of the TAC phenotype by its direct action on the expression of key cell cycle regulatory genes and also by regulating Wnt/b-catenin signalling activity. We also identify an essential requirement for TACs in maintaining the mesenchymal stem cells, indicative of a positive feedback mechanism. Analysing the properties of mesenchymal transit amplifying cells population and identifing key components of the molecular regulation that drives proliferation.

2019-03-12 | GSE104891 | GEO

Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor

Project description:Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor

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Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Microarray Expression]

Project description:Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Microarray Expression]

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Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Ring1b ChIP]

Project description:Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Ring1b ChIP]

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Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Histone ChIP]

Project description:Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Histone ChIP]

| PRJNA414106 | ENA

Gene expression profiling of murine incisor pulp following resection of the inferior alveolar nerve

Project description:The overall goal of this project is to investigate the contribution of the inferior alveolar nerve (IAN) towards cellular mechanisms required for regeneration of the murine incisor. Here, we conducted gene expression profiling of adult murine incisor dental mesenchyme tissue following two weeks after unilateral resection of the IAN from both the denerved and contralateral incisor of five wild-type mice.

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Six1 regulates mouse lower incisor development by coordinating Dlx1/2/5 [CUT&Tag]

Project description:Tooth development is a complex process orchestrated by intricate gene regulatory networks, involving both odontogenic epithelium and ectomesenchyme. Six1, a pivotal transcription factor (TF), is involved in the development of the lower incisor. However, its precise role during incisor development and the molecular mechanisms underpinning its regulatory functions remain poorly understood. This study employs Six1 deletion mouse models to elucidate the critical regulatory role of Six1 in governing dental mesenchyme development. By performing single-cell RNA sequencing (scRNA-seq), we constructed a comprehensive transcriptome atlas of tooth germ development from the bud to bell stage. Our analyses suggest that the dental follicle (DF) and the dental papilla (DP) are differentiated from dental ectomesenchyme (DEM), and identify the key transcription factors (TFs) underlying these distinct states. Notably, we show that Dlx1, Dlx2, and Dlx5 (Dlx1/2/5) may function as the key TFs that promote the formation of DP. We further show that the deletion of Six1 perturbs dental mesenchyme development by impeding the transitions from DEM to DP states. Importantly, SIX1 directly binds to the promoters of Dlx1/2/5 to promote their co-expression, which subsequently leads to widespread epigenetic and transcriptional remodeling. In summary, our findings unveil Six1's indispensable role in incisor development, offering key insights into transcription factor-driven regulatory networks that govern dental mesenchyme cell fate transitions during tooth development.

2024-05-06 | GSE254482 | GEO

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