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Transcriptional landscape of different brain regions in a Rett syndrome mouse model

ABSTRACT: We propose to investigate differential gene expression in Hippocampus and Frontal cortex of MeCP2 knock-out to gain more resolution on transcriptomic changes that occur in the Rett syndrome mouse model

ORGANISM(S): Mus musculus

PROVIDER: GSE60219 | GEO | 2018/09/30

REPOSITORIES: GEO

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Convergent Cerebrospinal Fluid Proteomes and Metabolic Ontologies in Humans and Animal Models of Rett Syndrome

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Project description:Rett syndrome (RTT) is a severe neurodevelopmental disorder that is caused by mutations in the gene methyl-CpG-binding-protein-2 (MECP2). However, the molecular mechanism by which these mutations mediate the RTT neuropathology remains enigmatic. In this study, we stimulated MeCP2-null cortical neurons (in vitro) and brains (in vivo) of a RTT mouse model to explore the effect of the loss of MeCP2 function on the activity-dependent transcriptomes of the cortex and hippocampus, respectively, using RNA-seq. These analyses revealed that the loss of MeCP2 results in aberrant global pattern of gene expression, characterized predominantly by higher levels of expression of activity-dependent genes, and anomalous alternative splicing events, specifically in response to neuronal activity.

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Neuronal cytoskeletal gene dysregulation drives mechanical hypersensitivity in Rett Syndrome

Project description:This study investigated mechanisms of peripheral sensory abnormalities in Rett Syndrome using a MeCP2 knockout rat. Dramatic changes in peripheral innervation by DRG sensory neurons were observed in the knockout rats that strongly correlated with modality-specific sensory dysfunction. The cell-autonomous effect of MeCP2 mutation in DRG neurons disrupt axon growth mechanisms leading to the altered cutaneous innervation density. We performed RNA-Seq to compare the transcriptome of MeCP2 KO DRGs with that derived from wildtype littermates. This revealed profound impact of MeCP2 loss on axon growth regulatory pathways in sensory neurons. The findings will have significant impact on our understanding of sensory dysfunctions in Rett syndrome and Autism Spectrum Disorders at large.

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