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Loss of non-CpG methylation in inhibitory neurons impairs neural function through a mechanism that partially overlaps with Rett syndrome

ABSTRACT: Loss of non-CpG methylation in inhibitory neurons impairs neural function through a mechanism that partially overlaps with Rett syndrome

PROVIDER: PRJNA510594 | ENA |

REPOSITORIES: ENA

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Loss of non-CpG methylation in inhibitory neurons impairs neural function through a mechanism that partially overlaps with Rett syndrome

Project description:Loss of non-CpG methylation in inhibitory neurons impairs neural function through a mechanism that partially overlaps with Rett syndrome

| PRJNA510359 | ENA

Loss of non-CpG methylation in inhibitory neurons impairs neural function through a mechanism that partially overlaps with Rett syndrome

Project description:Whole striatum were dissected from wild-type, as well as in mice where Dnmt3a or MeCP2 was conditional deleted in inhibitory neurons. Inhibitory neuronal nuclei were also conditionally tagged with GFP in all mice. Tissues were snap-frozen in liquid nitrogen until further analysis. Inhibitory neurons were sorted from whole striatum using anti-GFP-488 and anti-NeuN-647 signals and snap frozen until further analysis. Total DNA was purified from each sample using the DNeasy Blood & Tissue Kit from Qiagen according to manufactures instructions and stored at -20C until library preparation. DNA methylome libraries were generated using a modified snmC-seq method adapted for bulk DNA samples. Paired-end 150 cycle runs was used to sequence the libraries on a Illumina HiSeq 4000 Sequencing System.

2020-03-16 | GSE124009 | GEO

Loss of non-CpG methylation in inhibitory neurons impairs neural function through a mechanism that partially overlaps with Rett syndrome

Project description:Whole striatum were dissected from wild-type, as well as in mice where Dnmt3a or MeCP2 was conditional deleted in inhibitory neurons. Inhibitory neuronal nuclei were also conditionally tagged with GFP in all mice. Tissues were snap-frozen in liquid nitrogen until further analysis. Inhibitory neurons were sorted from whole striatum using anti-GFP-488 and anti-NeuN-647 signals and snap frozen until further analysis. Total nuclear RNA was purified from each sample using the Single Cell RNA Purification Kit from Norgen Biotek according to manufactures instructions and stored at -80C until library preparation at the Genomic and RNA Profiling Core at Baylor College of Medicine. NuGEN Ovation RNA-Seq v2 & Rubicon ThruPlex DNA-Seq kits were utilized for library preparation. A paired-end 100 cycle run was used to sequence the flowcell on a HiSeq 2500 Sequencing System.

2020-03-16 | GSE123941 | GEO

Long non-coding RNAs expression study of a Rett syndrome mouse model

Project description:In order to identify some lncRNA potentially involved in Rett syndrome we performed a mouse lncRNA expression microarray on whole brain samples coming from wild-type and MeCP2 Knock-out littermates. We found 2 lncRNAs directly bound by MeCP2 and upregulated in KO samples. We then focused on AK081227 because it overlaps with Gabrr2. The expression of this GABA receptor and the overlapping AK081227 are inversely correlated in thalamus, suggesting the long non-coding is regulating his own host. Whole brain total RNA was extracted from two Wild type mice (P60) and two MeCP2 KO littermates (P60)

2013-10-03 | E-GEOD-43689 | biostudies-arrayexpress

Long non-coding RNAs expression study of a Rett syndrome mouse model

2013-10-03 | GSE43689 | GEO

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.

2016-12-31 | GSE82068 | GEO

Transcriptome Analysis Of Human Rett Syndrome Brain

Project description:Transcriptome analysis of postmortem brain samples frrom frontal and temporal cortex of Rett Syndrome cases and matched controls. These data identify genes differentially expressed in postmortem brain tissue from Rett Syndrome cases. Total RNA was extracted from 100mg of postmortem brain tissue.

2015-11-24 | E-GEOD-75303 | biostudies-arrayexpress

Transcriptome Analysis Of Human Rett Syndrome Brain

2015-11-24 | GSE75303 | GEO

Epigenome analysis of Rett syndrome monozygotic twins samples

Project description:Genome wide DNA methylation profiling of Rett syndrome monozygotic twins. The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles in primary skin fibroblast cells from Rett syndrome monozygotic twins. Bisulphite converted DNA from the 2 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip

2012-12-27 | E-GEOD-43141 | biostudies-arrayexpress

Epigenome analysis of Rett syndrome monozygotic twins samples

2012-12-27 | GSE43141 | GEO

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