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Transcriptome analysis of different brain areas in Hcrt gene and Hcrt cell ablated mice

ABSTRACT: Transcriptome analysis of different brain areas in Hcrt gene and Hcrt cell ablated mice

PROVIDER: PRJNA521660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8555290.fastq.gz	Fastqsanger.gz
	SRR8555300.fastq.gz	Fastqsanger.gz
	SRR8555310.fastq.gz	Fastqsanger.gz
	SRR8555281.fastq.gz	Fastqsanger.gz
	SRR8555291.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of different brain areas in Hcrt gene and Hcrt cell ablated mice

Project description:Hypocretin (HCRT) and melanin concentrating hormone (MCH) are brain neuropeptides regulating a wide range of functions including sleep and metabolism. Loss of function of HCRT causes the sleep disorder narcolepsy. We found that loss of HCRT neurons in Hcrt-ataxin-3 mice results in a specific 50% decrease in another orexigenic neuropeptide QRFP that might explain the metabolic syndrome in narcolepsy.

2019-09-01 | GSE126345 | GEO

Brain areas involved with obsessive-compulsive disorder present different DNA methylation modulation

Project description:Background: Obsessive-compulsive disorder (OCD) is characterized by intrusive thoughts and repetitive actions, that presents the involvement of the cortico-striatal areas. The contribution of environmental risk factors to OCD development suggests that epigenetic mechanisms may contribute to its pathophysiology. DNA methylation changes and gene expression were evaluated in post-mortem brain tissues of the cortical (anterior cingulate gyrus and orbitofrontal cortex) and ventral striatum (nucleus accumbens, caudate nucleus and putamen) areas from eight OCD patients and eight matched controls. Results: There were no differentially methylated CpG (cytosine-phosphate-guanine) sites (DMSs) in any brain area, nevertheless gene modules generated from CpG sites and protein-protein-interaction (PPI) showed enriched gene modules for all brain areas between OCD cases and controls. All brain areas but nucleus accumbens presented a predominantly hypomethylation pattern for the differentially methylated regions (DMRs). Although there were common transcriptional factors that targeted these DMRs, their targeted differentially expressed genes were different among all brain areas. The protein-protein interaction network based on methylation and gene expression data reported that all brain areas were enriched for G-protein signaling pathway, immune response, apoptosis and synapse biological processes but each brain area also presented enrichment of specific signaling pathways. Finally, OCD patients and controls did not present significant DNA methylation age differences. Conclusions: DNA methylation changes in brain areas involved with OCD, especially those involved with genes related to synaptic plasticity and the immune system could mediate the action of genetic and environmental factors associated with OCD.

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RNAseq of 6 Different Rat Brain Areas after Treatment with a GLP-1 Receptor Agonist

Project description:In this study, we compared the treatment with one of 2 GLP-1 receptor agonists, Liraglutide and Semaglutide on the gene expression in 6 different DIO rat brain areas known to express the GLP-1 receptor. DIO rats were treated with vehicle, liraglutide, semaglutide or weight-matched for 23 days and tissue from the brain areas LS, PVH, ARH, DMH, AP and NTS was obtained with LCM.

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Brain areas involved with obsessive-compulsive disorder present different DNA methylation modulation

Project description:Brain areas involved with obsessive-compulsive disorder present different DNA methylation modulation

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RNA-seq of different brain tissue areas of Trrap conditional knockout Mus musculus

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Retina-derived signals control pace of neurogenesis in visual brain areas but not circuit configuration

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Gene expression from Prep1-ablated mice

Project description:The homeodomain transcription factor Prep1 was previously shown to regulate insulin sensitivity. Our aim was to study the specific role of Prep1 for the regulation of energy metabolism in skeletal muscle. Muscle specific ablation of Prep1 resulted in increased expression of respiratory chain subunits. This finding was consistent with an increase in mitochondrial enzyme activity without affecting mitochondrial volume fraction as assessed by electron microscopy. Metabolic phenotyping revealed no differences in daily energy expenditure or body composition. However, during treadmill exercise challenge, Prep1 ablation resulted in a higher maximal oxidative capacity and better endurance. Elevated PGC-1α expression was identified as a cause for increased mitochondrial capacity in Prep1-ablated mice. Prep1 stabilizes p160 Mybbp1a, a known inhibitor of PGC-1α activity. Thereby, P160 protein levels were significantly lower in muscle of Prep1-ablated mice. By a ChIPseq approach, PREP1-binding sites in genes encoding mitochondrial components (e.g. Ndufs2) were identified that might be responsible for elevated OXPHOS proteins in the muscle of Prep1 nullmutants. These results suggest that Prep1 exhibits additional direct effects on regulation of mitochondrial proteins. We therefore conclude that Prep1 is a regulator of oxidative phosphorylation components via direct and indirect mechanisms.

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