{"database":"ENA","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Fastqsanger.gz":["ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/001/SRR15711701/SRR15711701_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/099/SRR15711699/SRR15711699_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/001/SRR15711701/SRR15711701_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/000/SRR15711700/SRR15711700_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/004/SRR15711704/SRR15711704_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/003/SRR15711703/SRR15711703_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/000/SRR15711700/SRR15711700_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/002/SRR15711702/SRR15711702_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/099/SRR15711699/SRR15711699_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/004/SRR15711704/SRR15711704_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/002/SRR15711702/SRR15711702_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR157/003/SRR15711703/SRR15711703_2.fastq.gz"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Research center, The Seventh Affiliated Hospital, Sun Yat-sen University"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA760316"],"scientific_name":["Mus musculus"],"tag":["xref:PubMed:36131044"],"long_description":["Disrupted-in-schizophrenia-1 (DISC1), as one of the schizophrenia susceptibility genes highly expressed in oligodendrocyte precursor cells (OPCs), impacts oligodendroglial differentiation and myelination. Several DISC1 splicing variants, including DISC1-Δ3 (a DISC1 transcript with deleted exon 3 in a single allele), are abnormally upregulated in human schizophrenia patients, however, how they trigger the onset of the disease has not been explored yet. Here, we generate a mouse line that mimics human DISC1-Δ3 in oligodendrocyte lineage cells, and demonstrate that hypertrophic OPCs rather than myelin, are responsible for the neuronal deficits and schizophrenia-like symptoms. RNAseq was performed to analyze the transcriptome change in DISC1-Δ3 OPC, revealing that DISC1-Δ3 elevates the Wnt pathway activity in OPCs, which promotes Wif1 expression, thereby leading to disrupted synapse formation in neighboring neurons. Interfering or knockout of Wif1 in DISC1-Δ3 OPCs could rescue neuronal synaptic and functional deficits in our mouse model. Our findings shed light on the myelination-independent role of OPCs on the onset of schizophrenia, and may pave the way for new rational lines of inquiry in developing therapeutic strategies for schizophrenia. Overall design: RNA-seq was performed to understand the transcriptome change in DISC1-Δ3 forced expressed OPC in vivo Mice were divided in 2 groups: wt: control group. ko: NG2-CreERTM: DISC1 exon3 fl/+ (DISC1 ∆3) mice. Tamoxifen was given at the gavage for 4 consecutive days (p4-p7).On postnatal day 7, mice were sacrificed to isolate OPCs from the brain by pdgfrα immunopanning."],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"RNA-seq of oligodendroglia progenitor cells(OPCs) isolated from WT and DISC1-Δ3 mice","description":"RNA-seq of oligodendroglia progenitor cells(OPCs) isolated from WT and DISC1-Δ3 mice","dates":{"last_updated":"2025-09-24","first_public":"2023-01-27"},"accession":"PRJNA760316","cross_references":{"GEO":["GSE183341"],"taxon":["10090"],"PubMed":["36131044"]}}