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

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

PROVIDER: PRJNA839604 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19308800_1.fastq.gz	Fastqsanger.gz
	SRR19308800_2.fastq.gz	Fastqsanger.gz
	SRR19308801_1.fastq.gz	Fastqsanger.gz
	SRR19308801_2.fastq.gz	Fastqsanger.gz
	SRR19308802_1.fastq.gz	Fastqsanger.gz

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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 mutation mice age of postnatal day 10

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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.

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

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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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ARID1B

Project description:ARID1B

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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

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RNA-seq transcriptonal profiling in whole hippocampus in WT and Arid1b+/- mice

Project description:There is growing evidence for the involvement of ARID1B, a SWI/SNF ATP-dependent chromatin remodeling subunit, in a broad range of human disorders. Sequencing studies have recurrently implicated ARID1B haploinsufficiency in autism spectrum disorder (ASD), non-syndromic intellectual disability (ID), corpus callosum agenesis, and short stature. In addition, ARID1B is by far the most common cause of Coffin-Siris Syndrome (CSS), a monogenic developmental delay syndrome characterized by a combination of the neuropsychiatric and physical abnormalities mentioned above. To understand how ARID1B mutations lead to these phenotypes, we generated Arid1b mutant mice, which exhibited physical manifestations of developmental delay and behaviors reminiscent of ASD. In the brain, Arid1b haploinsufficiency resulted in changes in the expression of SWI/SNF- regulated genes implicated in ASD.

2017-06-26 | GSE92238 | GEO

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