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

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

PROVIDER: PRJNA839255 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19264200_1.fastq.gz	Fastqsanger.gz
	SRR19264200_2.fastq.gz	Fastqsanger.gz
	SRR19264201_1.fastq.gz	Fastqsanger.gz
	SRR19264201_2.fastq.gz	Fastqsanger.gz
	SRR19264192_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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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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