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Oxidative burden and mitochondrial dysfunction in a mouse model of Rett syndrome

ABSTRACT: To identify the detailed molecular causes of the mitochondrial dysfunction, oxidative burden and more vulnerable redox balance in Rett mouse hippocampus, we screened for differential gene expression in the hippocampal CA1 subfield of adult male mice. A whole mouse genome microarray was performed to assess, whether key enzymes of the mitochondrial respiratory chain or major cellular radical scavenging enzymes are affected in this MeCP2-deficient mouse model of Rett syndrome.

ORGANISM(S): Mus musculus

PROVIDER: GSE32870 | GEO | 2012/08/31

SECONDARY ACCESSION(S): PRJNA146559

REPOSITORIES: GEO

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Oxidative burden and mitochondrial dysfunction in a mouse model of Rett syndrome

Project description:To identify the detailed molecular causes of the mitochondrial dysfunction, oxidative burden and more vulnerable redox balance in Rett mouse hippocampus, we screened for differential gene expression in the hippocampal CA1 subfield of adult male mice. A whole mouse genome microarray was performed to assess, whether key enzymes of the mitochondrial respiratory chain or major cellular radical scavenging enzymes are affected in this MeCP2-deficient mouse model of Rett syndrome. Comparison of gene expression between male wildtype mice (Mecp2+/y) and mice lacking the MECP2 gene (Mecp2-/y) [B6.129P2(C)-Mecp2tm-1-1Bird (Guy et al. 2001, Nat. Genet. 27: 322-326)]. In total, 9 mice of each genotype were analyzed. The mRNA of groups of 3 animals was pooled to generate 3 independent biological samples, and finally three microarrays were run for each genotype.

2012-08-31 | E-GEOD-32870 | biostudies-arrayexpress

Negative allosteric modulation of mGluR5 partially corrects pathophysiology in a mouse model of Rett Syndrome

Project description:Rett syndrome is caused by mutations in the gene encoding methyl-CpG binding protein 2 (MECP2), an epigenetic regulator of mRNA transcription. Here we report a test of the hypothesis of shared pathophysiology of Rett syndrome and fragile X, another monogenic cause of autism and intellectual disability. In fragile X, the loss of the mRNA translational repressor FMRP leads to exaggerated protein synthesis downstream of metabotropic glutamate receptor 5 (mGluR5). We found that mGluR5- and protein synthesis-dependent synaptic plasticity is similarly altered in area CA1 of Mecp2 KO mice. CA1 pyramidal cell-type-specific, genome-wide profiling of ribosome-bound mRNAs was performed in wild-type and Mecp2 KO hippocampal CA1 neurons to reveal the MeCP2-regulated ‘translatome’. We found significant overlap between ribosome-bound transcripts overexpressed in the Mecp2 KO and FMRP mRNA targets. These tended to encode long genes that are functionally related to either cytoskeleton organization or the development of neuronal connectivity. In the Fmr1 KO mouse, chronic treatment with mGluR5 negative allosteric modulators (NAMs) has been shown to ameliorate many mutant phenotypes by correcting excessive protein synthesis. In the Mecp2 KO mice we found that mGluR5 NAM treatment significantly reduces the level of overexpressed ribosome-associated transcripts, particularly those that are also FMRP targets. Some Rett phenotypes were also ameliorated by treatment, most notably hippocampal cell size and life span. Together, these results suggest a potential mechanistic link between MeCP2-mediated transcription regulation and mGluR5/FMRP-mediated protein translation regulation through co-regulation of a subset of genes relevant to synaptic functions.

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Hippocampal Subfield Transcriptome Analysis in Schizophrenia Psychosis

Project description:We have previously demonstrated functional and molecular changes in hippocampal subfields in individuals with schizophrenia (SZ) psychosis associated with hippocampal excitability. In this study, we use RNA-seq and assess global transcriptome changes in the hippocampal subfields, DG, CA3, and CA1 from individuals with SZ psychosis and controls to elucidate subfield-relevant molecular changes. We also examine changes in gene expression due to antipsychotic medication in the hippocampal subfields from our SZ ON- and OFF-antipsychotic medication cohort. We identify unique subfield-specific molecular profiles in schizophrenia postmortem samples compared to controls, implicating astrocytes in DG, immune mechanisms in CA3, and synaptic scaling in CA1. We show a unique pattern of subfield-specific effects by antipsychotic medication on gene expression levels with scant overlap of genes differentially expressed by SZ disease effect versus medication effect. These hippocampal subfield changes could provide the basis for previously observed hippocampal SZ pathology and explain the lack of full efficacy of conventional antipsychotic medication on SZ symptomatology. With further characterization, the identified distinct molecular profiles of the DG, CA3, and CA1 in SZ psychosis may serve to identify potential hippocampal-based therapeutic targets.

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