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Whole-brain transcriptome of Arid1b heterozygote mutation mice age of postnatal day 3

ABSTRACT: Whole-brain transcriptome of Arid1b heterozygote mutation mice age of postnatal day 3

PROVIDER: PRJNA839057 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19243516_1.fastq.gz	Fastqsanger.gz
	SRR19243516_2.fastq.gz	Fastqsanger.gz
	SRR19243517_1.fastq.gz	Fastqsanger.gz
	SRR19243517_2.fastq.gz	Fastqsanger.gz
	SRR19243518_1.fastq.gz	Fastqsanger.gz

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Prefrontal cortex transcriptome of Arid1b heterozygote mutation mice age of postnatal day 10

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Whole-brain transcriptome of Arid1b heterozygote mutation mice age of postnatal day 3

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Prefrontal cortex transcriptome of Arid1b heterozygote mutation mice age of postnatal day 10

Project description:Prefrontal cortex transcriptome of Arid1b heterozygote mutation mice age of postnatal day 10

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Prefrontal cortex transcriptome of Arid1b heterozygote mutantation mice and drug treated-mice age of postnatal day 120

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Prefrontal cortex transcriptome of Arid1b heterozygote mutantation mice and drug treated-mice age of postnatal day 120

Project description:Prefrontal cortex transcriptome of Arid1b heterozygote mutantation mice and drug treated-mice age of postnatal day 120

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Brain transcriptome analysis of Arid1b heterozygote mutation and long-lasting effects of early chronic fluoxetine treatment for mutant mice [RNA-Seq]

Project description:Arid1b is a chromatin remodeler implicated in neurodevelopmental disorders. Arid1b mutant mice with haploinsufficiency (Arid1b HT) displayed persistent excitatory synaptic dysfunction from juvenile to adult stage, decreased synaptic density and transmission. Moreover, they showed autistic-like behaviors in both of early and adult stages, decreased sociability in pup USV calling and adult social interaction, and adult repetitive grooming. To investigate early transcriptomic changes in Arid1b mutant mice, RNAseq analysis of whole brain from wild-type and Arid1b mutant mice at postnatal day 10 was done. Transcriptomic changes support these electrophysiological and behavioral deficits. Arid1b HT mice at postnatal day 10 showed alterations in genes implicated in synaptic functions and ASD. Next, we found that early chronic fluoxetine treatment could carry out long-lasting restoration in electrophysiological and behavioral deficits in Arid1b HT mice. Whole brain transcriptomic analysis with mice at postnatal day 120 which underwent chronic fluoxetine treatment from postnatal day 3 to postnatal day 21 via mammillary milk was done to figure out transcriptomic reprogramming which contributes to this restoration. Comparing fluoxetine treated Arid1b HT mice and vehicle group, fluoxetine treated mice showed upregulation of synapse-related genes and disease related gene sets with reverse-ASD directions.

2022-07-21 | GSE189653 | GEO

ARID1B

Project description:ARID1B

| PRJEB30505 | ENA

Brain transcriptome analysis of Arid1b heterozygote mutation and long-lasting effects of early chronic fluoxetine treatment for mutant mice

Project description:Brain transcriptome analysis of Arid1b heterozygote mutation and long-lasting effects of early chronic fluoxetine treatment for mutant mice

| PRJNA839595 | 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

Brain transcriptome analysis of Arid1b heterozygote mutation and long-lasting effects of early chronic fluoxetine treatment for mutant mice [RNA-Seq]

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