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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: PRJNA510359 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8329200_1.fastq.gz	Fastqsanger.gz
	SRR8329200_2.fastq.gz	Fastqsanger.gz
	SRR8329210_1.fastq.gz	Fastqsanger.gz
	SRR8329210_2.fastq.gz	Fastqsanger.gz
	SRR8329220_1.fastq.gz	Fastqsanger.gz

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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

| PRJNA510594 | 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.

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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: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.

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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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Project description:Rett syndrome is an X-linked neurodevelopmental disorder caused by mutation in the methyl-CpG-binding protein 2 gene in the majority of cases. We describe an RNA sequencing dataset of postmortem brain tissue samples from four females clinically diagnosed with Rett syndrome and four age-matched female donors. The dataset contains transcriptomes from two brain regions, temporal and cingulate cortex, for each individual, providing a valuable resource to explore the biology of the human brain in Rett syndrome.

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

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Quantitative proteomic alterations of human iPSC-based neuronal development indicate early onset of Rett syndrome.

Project description:Rett syndrome (RTT) is a progressive neurodevelopmental disease often caused by mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MeCP2). The mechanisms by which impaired MeCP2 induces the pathological abnormalities in the brain is not understood. To understand the molecular mechanisms involved in disease onset, we used an RTT patient induced pluripotent stem cell (iPSC)-based model and applied an in-depth high-resolution quantitative mass spectrometry-based analysis during early stages of neuronal development. Our data provided evidence of proteomic alteration at developmental stages long before the phase that symptoms of RTT syndrome become apparent. Differential expression increased from early to late neural stem cell phases, although proteins involved in immunity, metabolic processes and calcium signaling were already affected at initial stages. This data can help development of new biomarkers and therapeutic approaches in RTT syndrome.

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Transcription profiling of human super frontal gyrus (post mortem brain) from Rett syndrome patients and age sex matched controls reveals FXYD1, an MeCP2 target gene overexpressed in the brains of Rett syndrome patients and Mecp2-null mice

Project description:Rett syndrome (RTT, OMIM 312750) is a severe X-linked neurodevelopmental disorder linked to heterozygous de novo mutations in the MECP2 gene. MECP2 encodes methyl-CpG-binding protein 2 (MeCP2), which represses gene transcription by binding to 5-methylcytosine residues in symmetrically positioned CpG dinucleotides. The disorder is almost exclusively diagnosed in females, because males affected by the disease usually die perinatally due to severe encephalopathy. Direct MeCP2 target genes underlying the neuropathogenesis of RTT remain largely unknown.

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Transcriptome Analysis Of Human Rett Syndrome Brain

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