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

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

PROVIDER: PRJNA599146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10832957_1.fastq.gz	Fastqsanger.gz
	SRR10832957_2.fastq.gz	Fastqsanger.gz
	SRR10832958_1.fastq.gz	Fastqsanger.gz
	SRR10832958_2.fastq.gz	Fastqsanger.gz
	SRR10832959_1.fastq.gz	Fastqsanger.gz

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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.

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Project description:To reveal the mechanisms of FGF13 in regulation of neural progenitor development, we carried out RNA-seq gene expression profiling analysis in primarily cultured hippocampal neurospheres from FGF13cko mice. 3 biological independent samples from FGF13cko (hGAFPCre+;Fgf13 flox/y) mice were compared with 3 independent litermate control (hGAFPCre+;Fgf13 +/y) samples.

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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.

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Impaired attenuation of pluripotency enhancers at the onset of neural crest formation in ARID1B haploinsufficient Coffin-Siris patients

Project description:De-novo ARID1B haploinsufficient mutations cause many developmental disorders characterized by neurological and craniofacial phenotypes, including Coffin-Siris Syndrome. ARID1B and its paralog ARID1A encode for mutually exclusive subunits of the BAF chromatin remodeler, yet their role in cell-fate determination is poorly understood. We discovered a novel neural crest configuration of the BAF complex (ARID1B-BAF), which includes ARID1B, SMARCA4, and eight additional subunits. The ARID1B-BAF regulates lineage commitment upon differentiation cues through attenuation of pluripotency enhancers of the SOX2 network. Consistently, the ARID1B-BAF interacts with SALL4, which is known to have repressing abilities during lineage commitment. In iPSCs, pluripotency enhancers are maintained in active state by cooperation between the pioneer activity of SOX2 and the ARID1A-containing BAF. At the onset of differentiation, ARID1B-BAF replaces ARID1A-BAF at these enhancers, eliciting chromatin repression and coordinating the exit from pluripotency. Coffin-Siris patient cells fail to perform the ARID1A/ARID1B switch, and maintain ARID1A-BAF at the pluripotency enhancers throughout CNCC differentiation. This correlates with aberrant SOX2 binding at the pluripotency enhancers, and failure to reposition SOX2 at the developmental enhancers. SOX2 dysregulation promotes upregulation of the NANOG regulatory network, impairing CNCC differentiation. Intriguingly, the patient with the most extreme molecular phenotype is also affected by a more severe version of the syndrome. These findings have significant biomedical implications, since they suggest a direct connection between ARID1B mutations and developmental disorders.

2021-09-22 | GSE169654 | GEO

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