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Comparing the cerebellar transcriptome of Sacs KO versus WT mice

ABSTRACT: Comparing the cerebellar transcriptome of Sacs KO versus WT mice

PROVIDER: PRJNA827122 | ENA |

REPOSITORIES: ENA

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Comparing the cerebellar transcriptome of Sacs KO versus WT mice

Project description:Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS) is caused by mutations in SACS gene encoding sacsin. ARSACS patients and mouse models display early degeneration of cerebellum in agreement with high sacsin expression in this organ. We performed unbiased transcriptomic of cerebella from Sacs KO mice versus controls to dissect the mechanisms underlying cerebellar degeneration in ARSACS.

2023-08-08 | GSE200876 | GEO

TRAP from CA1 pyramidal neurons and cerebellar granule cells in Fmr1 KO and wildtype mice

Project description:TRAP (translating ribosome affinity purification) from CA1 pyramidal neurons and cerebellar granule cells in wildtype and Fmr1 KO littermate pairs. These data show a global downregulation of FMRP targets in Fmr1 KO mice in these cell types.

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Project description:Transcriptional comparison of WT Tregs versus MOG KO Tregs

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Comparing the difference in gene expression between TDAG51 WT vs TDAG51 KO, and TDAG51 KO Tg vs TDAG51 KO

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E47 KO versus WT HSCs

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Mice lacking Astn2 have ASD-like behaviors and altered cerebellar circuit properties

Project description:Astrotactin 2 (ASTN2) is a transmembrane neuronal protein highly expressed in the cerebellum that functions in receptor trafficking and modulates cerebellar Purkinje cell (PC) synaptic activity. Individuals with ASTN2 mutations exhibit neurodevelopmental disorders, including autism spectrum disorder (ASD), ADHD, learning difficulties and language delay. To provide a genetic model for the role of the cerebellum in ASD-related behaviors and study the role of ASTN2 in cerebellar circuit function, we generated global and PC-specific conditional Astn2 knockout (KO and cKO, respectively) mouse lines. Astn2 KO mice exhibited strong ASD-related behavioral phenotypes, including a marked decrease in separation-induced pup ultrasonic vocalization calls, hyperactivity, and repetitive behaviors, altered behavior in the three-chamber test, and impaired cerebellar-dependent eyeblink conditioning. Hyperactivity and repetitive behaviors were also prominent in Astn2 cKO animals but they did not show altered behavior in the three-chamber test. By Golgi staining, Astn2 KO PCs had region-specific changes in dendritic spine density and filopodia numbers. Proteomic analysis of Astn2 KO cerebellum revealed a marked upregulation of ASTN2 family member, ASTN1, a neuron-glial adhesion protein. Immunohistochemistry and electron microscopy demonstrated a significant increase in Bergmann glia volume in the molecular layer of Astn2 KO animals. Electrophysiological experiments indicated a reduced frequency of spontaneous excitatory postsynaptic currents (EPSCs), as well as increased amplitudes of both spontaneous EPSCs and inhibitory postsynaptic currents (IPSCs) in the Astn2 KO animals, suggesting that pre- and postsynaptic components of synaptic transmission were altered. Thus, ASTN2 regulates ASD-like behaviors and cerebellar circuit properties.

2024-07-30 | PXD052868 | Pride

Single cell RNAseq of Th17 and Th22 cells with Gpr65_WT versus KO

Project description:scRNAseq of in vitro polarized Th17 and Th22 cells (Gpr65_WT versus KO), to compare metabolism gene expression in Gpr65_WT versus KO.

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ON and OFF SACs identified by scRNA-seq

Project description:The goal of this experiment was to investigate the heterogeneity of SACs via scRNA-seq

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Epigenome analysis of NNMT KO versus WT cells

Project description:Epigenome analysis of NNMT KO versus WT cells

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Proteomic datasets from sacsin knockout human SH-SY5Y and mouse primary cortical neurons

Project description:Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a childhood-onset cerebellar ataxia caused by mutations in SACS, which encodes the protein sacsin. Cellular ARSACS phenotypes include mitochondrial dysfunction, intermediate filament disorganization, and the progressive death of cerebellar Purkinje neurons. It is unclear how the loss of sacsin function causes these deficits, or why they manifest as cerebellar ataxia. Here, we performed multi-omic profiling in sacsin knockout (KO) cells, and identified alterations in microtubule dynamics, protein trafficking, and mislocalization of synaptic and focal adhesion proteins, including multiple integrins. Focal adhesion structure, signaling, and function were affected in KO cells, which could be rescued by reducing levels of PTEN, an overabundant negative regulator of focal adhesion signaling. Purkinje neurons in ARSACS mice possessed mislocalization of ITGA1, and disorganization of synaptic structures in the deep cerebellar nucleus (DCN). Interactome analysis revealed that sacsin regulates protein-protein interactions between structural and synaptic adhesion proteins. Our findings suggest that disrupted trafficking of synaptic adhesion proteins is a causal molecular deficit underlying ARSACS.

2022-10-25 | PXD036906 | Pride

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