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Mus musculus

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

PROVIDER: PRJNA304445 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2966780.fastq.gz	Fastqsanger.gz
	SRR2966790.fastq.gz	Fastqsanger.gz
	SRR2966781.fastq.gz	Fastqsanger.gz
	SRR2966791.fastq.gz	Fastqsanger.gz
	SRR2966782.fastq.gz	Fastqsanger.gz

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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

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).

2016-02-17 | E-GEOD-75510 | biostudies-arrayexpress

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

2016-02-17 | GSE75510 | GEO

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+/+).

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

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

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Mus musculus strain:B6.129

Project description:RNA sequencing - peritoneal macrophages congenic B6.129 mice lacking or expressing Prnp

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Prionic protein gene dosage is critical for maintenance of neuronal homeostasis of hippocampal circuits

Project description:We demonstrate that Prnp dosage is critical for the maintenance of neuronal homeostasis since both its absence and, more relevantly, its overexpression induce higher sensitivity to kainate (KA) damage. These data correlate with electrophysiological results in freely behaving mutant mice showing an imbalance in activity-dependent synaptic processes, as determined from input/output curves, paired-pulse facilitation, and LTP studies. Gene expression profiling showed that 129 genes involved in canonical pathways such as Ubiquitination or Neurotransmission among others were co-regulated in knockout and PrPc overexpressing mice. RT-qPCR analysis of neurotransmission-related genes confirmed GABA-A and AMPA-Kainate receptor subunit transcriptional co-regulation in both Prnp -/- and Tg20 mice. Our results demonstrate that PrPc is necessary for the proper homeostatic functioning of hippocampal circuits, because of its interactions with GABAA and AMPA-Kainate receptors. Keywords: steady state expression; adult brain tissue; hippocampus; genetic modification; transgenic gain of function mutation; targetted deletion loss of function mutation We performed a global transcriptome analysis of three strains that differ in their Prnp gene dose using Illumina Sentrix 6 mouse v1.1 beadarrays. We analyzed mRNA expression in the hippocampi of four individual male mice from each of three strains: 1) Tg20, with a 30 exogenous copies of the Prnp gene within a Prnp -/- background that overexpresses PrPc about 6-7 times the normal wild type levels; 2) littermates lacking the transgene and therefore carrying only the homozygous knock out Prnp -/- strain which lacks expression of PrPc; and 3) their wild type counterparts carrying two copies of the intact Prnp gene and expressing normal levels of PrPc

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Gene expression analysis in Fmr1KO mice identifies an immunological signature in brain tissue and mGluR5-related signaling in primary neuronal cultures.

Project description:Transcriptome profile of whole tissue and cultured neuronal cells from the hippocampus and cortex from pooled littermate embryos (at 17-18 days post conception) of 2 mouse genotypes C57BL/6 congenic WT and Fmr1 KO.

2015-12-13 | GSE71034 | GEO

Congenic dissection of a major QTL for methamphetamine sensitivity implicates epistasis

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Prionic protein gene dosage is critical for maintenance of neuronal homeostasis of hippocampal circuits

2010-01-08 | GSE16223 | GEO

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Project description:Diabetic kidney disease (DKD) appears heritable, suggesting genetic factors influence disease susceptibility. In our study, genes were mapped mediating early renal hypertrophic in response to diabetes. A survey of murine strains (N=15) was conducted to identify variation in kidney hypertrophy following diabetes induction. Mice with greater FVB/N and less C57BL/6 renal hypertrophy were crossed and diabetic F2 generation mice (n=534) were characterised. To confirm loci responsible for the renal hypertrophic response, diabetic congenic mice were generated by backcrossing FVB/N mice that conferred greater or C57BL/6 conferring lower risk into the reciprocal strain mice. Kidney weights of (FVB/N x C57BL/6) F2 diabetic mice were broadly distributed. Quantitative trait locus (QTL) analysis revealed that diabetic mice with kidney weights in the upper quartile shared alleles on chromosomes 6 and 12, with the FVB/N allele on chromosome 6 conferring greater susceptibility. On chromosome 12, C57BL/6 homozygotes were more significantly represented (LOD=3.8) conferring less susceptibility. The diabetic B6.Drc1/2f congenic strain developed kidney damage, while the reciprocal congenic, with FVB.Drc1/2b strain were protected. Microarray analysis identified differentially expressed genes between diabetic C57BL/6 and FVB/N mice. QTL mapping for early renal responses to diabetes identified two loci syntenic with regions identified for human diabetic kidney disease. Providing a new resource to study DKD.

2021-12-31 | GSE123677 | GEO

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