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Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [ChIP-Seq]

ABSTRACT: Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [ChIP-Seq]

PROVIDER: PRJNA700605 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13651938.fastq.gz	Fastqsanger.gz
	SRR13651939.fastq.gz	Fastqsanger.gz

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Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [RNA-Seq]

Project description:We show that loss of Arid1a impairs the differentiation-associated cell cycle arrest of tooth root progenitors through Hh signaling regulation, leading to shortened roots. Our data suggest that Plagl1, as a cofactor, endows Arid1a with its cell type/spatial functional specificity.

2021-04-04 | GSE166358 | GEO

Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [ChIP-Seq]

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Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [ATAC-Seq]

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Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors

Project description:Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors

| PRJNA700598 | ENA

Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [ATAC-Seq]

Project description:Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [ATAC-Seq]

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Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [RNA-Seq]

Project description:Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors [RNA-Seq]

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Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors.

Project description:Chromatin remodelers often show broad expression patterns in multiple cell types yet can elicit cell-specific effects in development and diseases. Arid1a binds DNA and regulates gene expression during tissue development and homeostasis. However, it is unclear how Arid1a achieves its functional specificity in regulating progenitor cells. Using the tooth root as a model, we show that loss of Arid1a impairs the differentiation-associated cell cycle arrest of tooth root progenitors through Hedgehog (Hh) signaling regulation, leading to shortened roots. Our data suggest that Plagl1, as a co-factor, endows Arid1a with its cell-type/spatial functional specificity. Furthermore, we show that loss of Arid1a leads to increased expression of Arid1b, which is also indispensable for odontoblast differentiation but is not involved in regulation of Hh signaling. This study expands our knowledge of the intricate interactions among chromatin remodelers, transcription factors, and signaling molecules during progenitor cell fate determination and lineage commitment.

| S-EPMC8132592 | biostudies-literature

Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-04-04 | GSE166360 | GEO

Progressive Tooth Pattern Changes in Cilk1-Deficient mice Depending on Hedgehog Signaling

Project description:Primary cilia function as critical sensory organelles that mediate multiple signaling pathways, including the Hedgehog (Hh) pathway, which is essential for organ patterning and morphogenesis. Disruptions in Hh signaling have been implicated in supernumerary tooth formation and molar fusion in mutant mice. Cilk1, a highly conserved serine/threonine-protein kinase localized within primary cilia, plays a critical role in ciliary transport. Loss of Cilk1 results in severe ciliopathy phenotypes, including polydactyly, edema, and cleft palate. However, the role of Cilk1 in tooth development remains unexplored. In this study, we investigated the role of Cilk1 in tooth development. Cilk1 deficiency resulted in downregulation of Hh target genes, leading to the formation of supernumerary teeth. This study reveals a previously unrecognized role of Cilk1 in controlling tooth morphology via Hh signaling.

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Project description:This study aimed to perform transcriptome profiling of Nfic-/- and corresponding control tooth germ at root initiation stage to identify differentially expressed for key regulators of root development. Coordination between the Hertwig’s Epithelial Root Sheath (HERS) and apical papilla (AP) is crucial for proper root development process. The Hedgehog (Hh) signaling pathway and Nfic are both involved in tooth root development.

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