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Arid1a regulates cell cycle exit of transit-amplifying cells through inhibiting the Aurka-Cdk1 axis in mouse incisor

ABSTRACT: We show that Arid1a maintains tissue homeostasis through promoting cell cycle exit and differentiation of TACs by inhibiting the Aurka-Cdk1 axis.

ORGANISM(S): Mus musculus

PROVIDER: GSE166800 | GEO | 2021/04/04

REPOSITORIES: GEO

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Arid1a regulates cell cycle exit of transit-amplifying cells by inhibiting the Aurka-Cdk1 axis in mouse incisor.

Project description:Stem cells self-renew or give rise to transit-amplifying cells (TACs) that differentiate into specific functional cell types. The fate determination of stem cells to TACs and their transition to fully differentiated progeny is precisely regulated to maintain tissue homeostasis. Arid1a, a core component of the switch/sucrose nonfermentable complex, performs epigenetic regulation of stage- and tissue-specific genes that is indispensable for stem cell homeostasis and differentiation. However, the functional mechanism of Arid1a in the fate commitment of mesenchymal stem cells (MSCs) and their progeny is not clear. Using the continuously growing adult mouse incisor model, we show that Arid1a maintains tissue homeostasis through limiting proliferation, promoting cell cycle exit and differentiation of TACs by inhibiting the Aurka-Cdk1 axis. Loss of Arid1a overactivates the Aurka-Cdk1 axis, leading to expansion of the mitotic TAC population but compromising their differentiation ability. Furthermore, the defective homeostasis after loss of Arid1a ultimately leads to reduction of the MSC population. These findings reveal the functional significance of Arid1a in regulating the fate of TACs and their interaction with MSCs to maintain tissue homeostasis.

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Arid1a regulates cell cycle exit of transit-amplifying cells through inhibiting the Aurka-Cdk1 axis in mouse incisor

Project description:Arid1a regulates cell cycle exit of transit-amplifying cells through inhibiting the Aurka-Cdk1 axis in mouse incisor

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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 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.

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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 [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.

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Transit amplifying cells coordinate mouse incisor mesenchymal stem cell activation.

Project description:Stem cells (SCs) receive inductive cues from the surrounding microenvironment and cells. Limited molecular evidence has connected tissue-specific mesenchymal stem cells (MSCs) with mesenchymal transit amplifying cells (MTACs). Using mouse incisor as the model, we discover a population of MSCs neibouring to the MTACs and epithelial SCs. With Notch signaling as the key regulator, we disclose molecular proof and lineage tracing evidence showing the distinct MSCs contribute to incisor MTACs and the other mesenchymal cell lineages. MTACs can feedback and regulate the homeostasis and activation of CL-MSCs through Delta-like 1 homolog (Dlk1), which balances MSCs-MTACs number and the lineage differentiation. Dlk1's function on SCs priming and self-renewal depends on its biological forms and its gene expression is under dynamic epigenetic control. Our findings can be validated in clinical samples and applied to accelerate tooth wound healing, providing an intriguing insight of how to direct SCs towards tissue regeneration.

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Regulation of Mesenchymal Stem to Transit-Amplifying Cell Transition in the Continuously Growing Mouse Incisor.

Project description:In adult tissues and organs with high turnover rates, the generation of transit-amplifying cell (TAC) populations from self-renewing stem cells drives cell replacement. The role of stem cells is to provide a renewable source of cells that give rise to TACs to provide the cell numbers that are necessary for cell differentiation. Regulation of the formation of TACs is thus fundamental to controlling cell replacement. Here, we analyze 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 by regulating Wnt/β-catenin-signaling activity. We also identify an essential requirement for TACs in maintaining mesenchymal stem cells, which is indicative of a positive feedback mechanism.

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Identification of genes are regulated by AURKA at transcription level

Project description:Purpose: AURKA plays an important role in breast cancer development. Exploring the gene expression profiles regulated by AURKA will facilitate to understand the mechanism which is responsible for AURKA induced breast cancer development. Results: We found that 350 genes were significantly up-regulated during AURKA overexpression in MCF-10A cells, 346 genes were significantly down-regulated during AURKA overexpression in MCF-10A cells. Conclusions: Our study indicated that 696 differentially expressed genes might contribute to AURKA induced breast cancer development. MCF-10A cells overexpressed AURKA or the empty vector were subjected to RNA extraction. The resulted RNA samples were performed RNA-sequencing analyses of gene expression profiles.

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Project description:To gain insight into genes regulated by AURKA, AURKA was knocked down (KD) in MDA-MB-231 cells

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