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

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

PROVIDER: PRJNA700598 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13651932_1.fastq.gz	Fastqsanger.gz
	SRR13651932_2.fastq.gz	Fastqsanger.gz
	SRR13651933_1.fastq.gz	Fastqsanger.gz
	SRR13651933_2.fastq.gz	Fastqsanger.gz
	SRR13651934_1.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.

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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 [ChIP-Seq]

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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]

| PRJNA700603 | ENA

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 [ChIP-Seq]

Project description: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.

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

An Nfic-Hedgehog Signaling Cascade Regulates Tooth Root Development

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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Project description:Retinal damage triggers reactive gliosis in Müller glia across vertebrate species, but only in regenerative animals, such as teleost fish, do Müller glia initiate repair; proliferating and undergoing neurogenesis to replace lost cells. We found that Plagl1, a maternally imprinted gene, is dynamically regulated in reactive Müller glia post-insult, with transcript levels transiently increasing before stably declining. To study Plagl1 retinal function, we examined Plagl1+/-pat null mutants postnatally, revealing defects in retinal architecture, visual signal processing and a reactive gliotic phenotype. Plagl1+/-pat Müller glia proliferate ectopically and give rise to inner retinal neurons and photoreceptors. Transcriptomic and ATAC-seq profiles revealed similarities between Plagl1+/-pat retinas and neurodegenerative and injury models, including an upregulation of pro-gliogenic and pro-proliferative pathways, such as Notch, not observed in wild-type retinas Plagl1 is thus an essential component of the transcriptional regulatory networks that retain mammalian Müller glia in quiescence.

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