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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE237303 | 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 [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:This SuperSeries is composed of the SubSeries listed below.

2024-03-20 | GSE237305 | GEO

ARID1B

Project description:ARID1B

| PRJEB30505 | ENA

Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders

Project description:The BAF complex modulates chromatin accessibility. Specific BAF configurations have functional consequences, and subunit switches are essential for cell differentiation. ARID1B and its paralog ARID1A encode for mutually exclusive BAF subunits. De novo ARID1B haploinsufficient mutations cause a neurodevelopmental disorder spectrum, including Coffin-Siris syndrome, which is characterized by neurological and craniofacial features. Here, we reprogrammed ARID1B+/- Coffin-Siris patient-derived skin fibroblasts into iPSCs, and modeled cranial neural crest cell (CNCC) formation. We discovered that ARID1B is active only during the first stage of this process, coinciding with neuroectoderm specification, where it is part of a lineage-specific BAF configuration (ARID1B-BAF), including SMARCA4, and nine additional subunits. ARID1B-BAF acts as a gate-keeper, ensuring exit from pluripotency and lineage commitment, by attenuating NANOG, SOX2 and the thousands of enhancers directly regulated by these two pluripotency factors at the iPSC stage. In iPSCs, these enhancers are maintained active by an ARID1A-containing BAF. At the onset of differentiation, cells transition from ARID1A-BAF to ARID1B-BAF, eliciting attenuation of the NANOG/SOX2 networks, and triggering pluripotency exit. Coffin-Siris patient cells fail to perform the ARID1A/ARID1B switch, and maintain ARID1A-BAF at pluripotency enhancers throughout all stages of CNCC formation. This leads to a persistent and aberrant SOX2 and NANOG activity, which impairs CNCC formation. In fact, despite showing the typical neural crest signature (TFAP2A+, SOX9+), the ARID1B-haploinsufficient CNCCs are also NANOG-positive, in stark contrast with the ARID1B-wt CNCCs, which are NANOG-negative. These findings suggest a connection between ARID1B mutations, neuroectoderm formation, and a pathogenic mechanism for Coffin-Siris syndrome.

2021-10-12 | PXD028557 | Pride

Arid1b ChIP-seq

Project description:Arid1b ChIP-seq

2022-12-25 | GSE214879 | GEO

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

Project description: Not available

| S-EPMC7461627 | biostudies-literature

RNA-seq analysis upon ARID1B overexpression

Project description:We transduced either an empty vector or ARID1B cDNA in IMR90 cells. Cells were selected with puromycin and 6 days after the infection we collected the RNA. ARID1B is a member of the SWI/SNF chromatin-remodeling complex. Our previous experiments showed that knockdown of ARID1B allows cells to bypass cellular senescence. By performing RNA-seq we have shown that ARID1B expression can induce a set of genes involved in the senescence response.

2016-11-12 | GSE75291 | GEO

Six1 regulates mouse lower incisor development by coordinating Dlx1/2/5 [scRNA-seq]

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 | GSE254658 | GEO

RNA-seq analysis of primarily cultured neurospheres from ARID1B haploinsufficient and control mice

Project description:To identify ARID1B associated genes in development of neural progenitor , we carried out RNA-seq gene expression profiling analysis in primarily cultured neurospheres from ARID1B haploinsufficient and control mice. 3 biological independent sample from ARID1B hi (hGAFPCre+;ARID1B flox/+) mice were compared with 2 independent litermate control (hGAFPCre+; ARID1B +/+) samples.

2021-01-07 | GSE143171 | GEO

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