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

PROVIDER: PRJNA994544 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25265432_1.fastq.gz	Fastqsanger.gz
	SRR25265432_2.fastq.gz	Fastqsanger.gz
	SRR25265433_1.fastq.gz	Fastqsanger.gz
	SRR25265433_2.fastq.gz	Fastqsanger.gz

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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 [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: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 [scATAC-seq]

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

| PRJNA994546 | ENA

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]

| PRJNA994545 | ENA

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

BCL11B

Project description:BCL11B

| PRJNA330816 | 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

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