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RNA sequencing of hippocampus of Prnp+/+ and PrnpZH3/ZH3 animals

ABSTRACT: RNA sequencing of hippocampus of Prnp+/+ and PrnpZH3/ZH3 animals

PROVIDER: PRJNA784185 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17054578.fastq.gz	Fastqsanger.gz
	SRR17054579.fastq.gz	Fastqsanger.gz
	SRR17054580.fastq.gz	Fastqsanger.gz
	SRR17054581.fastq.gz	Fastqsanger.gz
	SRR17054582.fastq.gz	Fastqsanger.gz

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RNA sequencing of hippocampus of Prnp+/+ and PrnpZH3/ZH3 animals

Project description:Purpose: Gain insight into the gene expression patterns altered in the PrnpZH3/ZH3 mice, that correleate with their neurobehavioural impaiments. Results: Around 700 genes showed alterations in their expression profile (323 upregulated and 390 downregulated in PrnpZH3/ZH3 compared to Prnp+/+).

2021-12-05 | GSE189691 | GEO

Impact of Prnp genetic ablation in the hippocampus transcriptome of congenic B6.129-PrnpZH1/ZH1 or coisogenic C57BL/6-PrnpZH3/ZH3 mice

Project description:To study the effect of Prnp genetic ablation on different aspects of RNA metabolism, we performed RNA sequencing of the hippocampus of wild-type C57BL/6J, congenic B6.129-PrnpZH1/ZH1 and coisogenic C57BL/6J-PrnpZH3/ZH3 mice. We analyzed differential gene expression, exon usage and RNA editing. RNA sequencing on hippocampus of wild-type C57BL/6 mice, congenic B6.129-PrnpZH1/ZH1 and coisogenic C57BL/6-PrnpZH3/ZH3 mice (3 month-old males, n=4 per genotype).

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Impact of Prnp genetic ablation in the hippocampus transcriptome of congenic B6.129-PrnpZH1/ZH1 or coisogenic C57BL/6-PrnpZH3/ZH3 mice

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Project description:We performed RNA sequencing for hippocampus of neonatal mice that were exposed to sevoflurane. We treated a group of neonatal mice with 2.5% sevoflurane for 2 hours on day 6, 7, 8, 9 and treated another group on day 6, 7. On day 36, we collected RNA (both total RNA and polysome-associated RNA) from the hippocampus in the aforementioned two groups and the control group (i.e., without sevoflurane treatment). We prepared the sequencing libraries with the collected RNA and sent them to Illumina sequencing platform.

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RNA sequencing in the ventral hippocampus

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RNA sequencing of sciatic nerves from ZH3 and WT mice

Project description:The transcriptome of sciatic nerves was investigated by RNA sequencing. We compared the transcriptome of ZH3 sciatic nerves to WT sciatic nerves in two age groups. Differentially expressed genes were considered as indicators of peripheral nerve damage in ZH3 mice. Then, we compared the sciatic nerve transcriptome of ZH3 mice chronically treated with a dimeric PrP-fusion protein (FT2Fc) to the two control groups treated with either buffer or mouse IgG. This comparison revealed specific changes induced by FT2Fc treatment. Contrary to our hypothesis, FT2Fc treatment did not alter the expression of the genes that were dysregulated in young and old ZH3 mice (as identified in the first part of the study).

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Project description:Wolfram syndrome is caused by mutations in the WFS1 gene. WFS1 protein dysfunction results in a range of neuroendocrine syndromes and is mostly characterized by juvenile-onset diabetes mellitus and optic atrophy. WFS1 has been shown to participate in membrane trafficking, protein processing and Ca2+ homeostasis in the endoplasmic reticulum. In the present study we aimed to find the transcriptomic changes influenced by Wfs1 in the hypothalamus and hippocampus using RNA-sequencing. We used WFS1-deficient mice as a model system to analyze the changes in transcriptional networks. The number of differentially expressed genes between hypothalami of WFS1-deficient (Wfs1KO) and wild-type (WT) mice was 43 and between hippocampi 311 with False Discovery Rate (FDR) <0.05. In hypothalamus of Wfs1KO mice one of the most upregulated genes was Avpr1a whilst Avpr1b was significantly upregulated in hippocampus. Trpm8 was the most upregulated gene in the hippocampus of Wfs1KO mice. The functional analysis revealed significant enrichment of networks and pathways associated with protein synthesis, cell-to-cell signaling and interaction, molecular transport, metabolic disease and nervous system development and function. In conclusion, the transcriptomic profiles of WFS1-deficient hypothalamus and hippocampus do indicate the activation of degenerative molecular pathways causing the clinical occurrences typical to Wolfram syndrome.

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