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ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE237305 | GEO | 2024/03/20

REPOSITORIES: GEO

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ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [scATAC-seq]

Project description:ARID1B is a epigenetic regulator. We used the scATAC sequencing to analysis the role of ARID1B in regulating mouse incisor tissue homeostasis.

2024-03-20 | GSE237304 | GEO

ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [scRNA-seq]

Project description:ARID1B is a epigenetic regulator. We used the scRNA sequencing to analysis the role of ARID1B in regulating mouse incisor tissue homeostasis.

2024-03-20 | GSE237303 | GEO

ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [bullk RNA-seq]

Project description:ARID1B is a epigenetic regulator. We used the RNA sequencing to analysis the role of ARID1B in regulating mouse incisor tissue homeostasis.

2024-03-20 | GSE237302 | GEO

ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor.

Project description:ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor.

| PRJNA994543 | ENA

ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [scRNA-seq]

Project description:ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [scRNA-seq]

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ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [scATAC-seq]

Project description:ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [scATAC-seq]

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ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [bullk RNA-seq]

Project description:ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [bullk RNA-seq]

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Runx2+ Niche Cells Maintain Incisor Mesenchymal Tissue Homeostasis through IGF Signaling.

Project description:Stem cell niches provide a microenvironment to support the self-renewal and multi-lineage differentiation of stem cells. Cell-cell interactions within the niche are essential for maintaining tissue homeostasis. However, the niche cells supporting mesenchymal stem cells (MSCs) are largely unknown. Using single-cell RNA sequencing, we show heterogeneity among Gli1+ MSCs and identify a subpopulation of Runx2+/Gli1+ cells in the adult mouse incisor. These Runx2+/Gli1+ cells are strategically located between MSCs and transit-amplifying cells (TACs). They are not stem cells but help to maintain the MSC niche via IGF signaling to regulate TAC proliferation, differentiation, and incisor growth rate. ATAC-seq and chromatin immunoprecipitation reveal that Runx2 directly binds to Igfbp3 in niche cells. This Runx2-mediated IGF signaling is crucial for regulating the MSC niche and maintaining tissue homeostasis to support continuous growth of the adult mouse incisor, providing a model for analysis of the molecular regulation of the MSC niche.

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BCL11B regulates epithelial proliferation and asymmetric development of the mouse mandibular incisor.

Project description:Mouse incisors grow continuously throughout life with enamel deposition uniquely on the outer, or labial, side of the tooth. Asymmetric enamel deposition is due to the presence of enamel-secreting ameloblasts exclusively within the labial epithelium of the incisor. We have previously shown that mice lacking the transcription factor BCL11B/CTIP2 (BCL11B hereafter) exhibit severely disrupted ameloblast formation in the developing incisor. We now report that BCL11B is a key factor controlling epithelial proliferation and overall developmental asymmetry of the mouse incisor: BCL11B is necessary for proliferation of the labial epithelium and development of the epithelial stem cell niche, which gives rise to ameloblasts; conversely, BCL11B suppresses epithelial proliferation, and development of stem cells and ameloblasts on the inner, or lingual, side of the incisor. This bidirectional action of BCL11B in the incisor epithelia appears responsible for the asymmetry of ameloblast localization in developing incisor. Underlying these spatio-specific functions of BCL11B in incisor development is the regulation of a large gene network comprised of genes encoding several members of the FGF and TGFβ superfamilies, Sprouty proteins, and Sonic hedgehog. Our data integrate BCL11B into these pathways during incisor development and reveal the molecular mechanisms that underlie phenotypes of both Bcl11b(-/-) and Sprouty mutant mice.

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Non-canonical functions of UHRF1 maintain DNA methylation homeostasis in cancer cells.

Project description:DNA methylation is an essential epigenetic chromatin modification, and its maintenance in mammals requires the protein UHRF1. It is yet unclear if UHRF1 functions solely by stimulating DNA methylation maintenance by DNMT1, or if it has important additional functions. Using degron alleles, we show that UHRF1 depletion causes a much greater loss of DNA methylation than DNMT1 depletion. This is not caused by passive demethylation as UHRF1-depleted cells proliferate more slowly than DNMT1-depleted cells. Instead, bioinformatics, proteomics and genetics experiments establish that UHRF1, besides activating DNMT1, interacts with DNMT3A and DNMT3B and promotes their activity. In addition, we show that UHRF1 antagonizes active DNA demethylation by TET2. Therefore, UHRF1 has non-canonical roles that contribute importantly to DNA methylation homeostasis; these findings have practical implications for epigenetics in health and disease.

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