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Whole transcriptome sequencing of E18 mouse cortex

ABSTRACT: We observed Csmd3-deficient mice exhibited growth retardation, atypical learning and memory behaviors. Futher, cortical neurons from mice lacking Csmd3 showed abnormal development. To identified the role of Csmd3 in cortex develepement, we performed whole transcriptome sequencing on embryonic 18 days cortex from Csmd3-/- and wild type mice. As a result, a total of 2133 differentially expressed genes (DEGs) were identified, including 1400 upregulated genes and 733 downregulated genes. Downregulated DEGs were mainly related to synaptic functions, while the upregulated DEGs were involved in multiple progresses related to cell-to-cell communication. In terms of cell type preference as referring to the single cell sequencing data in mouse neocortex at E18, downregulated DEGs were exlusively enriched into neurons and upregulated DEGs were involved with multiple cell types. Our study is the first detailed analyses of Csmd3 in development mouse cortex, identifing Csmd3 plays a pivotal role in synaptic organazation and transmission, also has an effect on glia-vascular inter-cellular communication.

ORGANISM(S): Mus musculus

PROVIDER: GSE186561 | GEO | 2022/03/05

REPOSITORIES: GEO

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Project description:<h4><strong>INTRODUCTION: </strong>Approximately 1% of the world's population is impacted by epilepsy, a chronic neurological disorder characterized by seizures. One-third of epileptic patients are resistant to AEDs, or have medically refractory epilepsy (MRE). One non-invasive treatment that exists for MRE includes the ketogenic diet, a high-fat, low-carbohydrate diet. Despite the KD's success in seizure attenuation, it has a few risks and its mechanisms remain poorly understood. The KD has been shown to improve metabolism and mitochondrial function in epileptic phenotypes. Potassium channels have implications in epileptic conditions as they have dual roles as metabolic sensors and control neuronal excitation.</h4><h4><strong>OBJECTIVES: </strong>The goal of this study was to explore changes in the lipidome in hippocampal and cortical tissue from Kv1.1-KO model of epilepsy.</h4><h4><strong>METHODS: </strong>FT-ICR/MS analysis was utilized to examine nonpolar metabolome of cortical and hippocampal tissue isolated from a Kv1.1 channel knockout mouse model of epilepsy (n = 5) and wild-type mice (n = 5).</h4><h4><strong>RESULTS: </strong>Distinct metabolic profiles were observed, significant (p < 0.05) features in hippocampus often being upregulated (FC ≥ 2) and the cortex being downregulated (FC ≤ 0.5). Pathway enrichment analysis shows lipid biosynthesis was affected. Partition ratio analysis revealed that the ratio of most metabolites tended to be increased in Kv1.1-/-. Metabolites in hippocampal tissue were commonly upregulated, suggesting seizure initiation in the hippocampus. Aberrant mitochondrial function is implicated by the upregulation of cardiolipin, a common component in the mitochondrial membrane.</h4><h4><strong>CONCLUSION: </strong>Generally, our study finds that the lipidome is changed in the hippocampus and cortex in response to Kv1.1-KO indicating changes in membrane structural integrity and synaptic transmission.</h4>

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Whole transcriptome sequencing of E18 mouse cortex

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