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Genome-wide transcriptomics identifies an early preclinical signature of prion infection

ABSTRACT: Genome-wide transcriptomics identifies an early preclinical signature of prion infection

PROVIDER: PRJNA604764 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11017800_1.fastq.gz	Fastqsanger.gz
	SRR11017800_2.fastq.gz	Fastqsanger.gz
	SRR11017900_1.fastq.gz	Fastqsanger.gz
	SRR11017900_2.fastq.gz	Fastqsanger.gz
	SRR11017801_1.fastq.gz	Fastqsanger.gz

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Genome-wide transcriptomics identifies an early preclinical signature of prion infection

Project description:We constructed a searchable genome-wide atlas of mRNA abundance, splicing and editing alterations during the course of disease in prion-inoculated mice.

2020-06-12 | GSE144738 | GEO

Genome-wide transcriptomics identifies an early preclinical signature of prion infection.

Project description:The clinical course of prion diseases is accurately predictable despite long latency periods, suggesting that prion pathogenesis is driven by precisely timed molecular events. We constructed a searchable genome-wide atlas of mRNA abundance and splicing alterations during the course of disease in prion-inoculated mice. Prion infection induced PrP-dependent transient changes in mRNA abundance and processing already at eight weeks post inoculation, well ahead of any neuropathological and clinical signs. In contrast, microglia-enriched genes displayed an increase simultaneous with the appearance of clinical signs, whereas neuronal-enriched transcripts remained unchanged until the very terminal stage of disease. This suggests that glial pathophysiology, rather than neuronal demise, could be the final driver of disease. The administration of young plasma attenuated the occurrence of early mRNA abundance alterations and delayed signs in the terminal phase of the disease. The early onset of prion-induced molecular changes might thus point to novel biomarkers and potential interventional targets.

| S-EPMC7360066 | biostudies-literature

Single-cell transcriptomics of mammalian prion diseases identifies dynamic gene signatures shared between species [mouse_scRNAseq]

Project description:Mammalian prion diseases are fatal and transmissible neurological conditions caused by the propagation of prions, self-replicating multimeric assemblies of misfolded forms of host cellular prion protein. Despite extensive studies investigating the changes in transcriptional profiles in prion diseases the mechanisms by which prion diseases induce cellular toxicity, including changes in gene expression profiles are yet to be fully characterized. Here, we took advantage of the recent developments in single-cell technologies and performed an unbiased whole-transcriptome single-nucleus transcriptomic analysis in prion disease.

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Single-cell transcriptomics of mammalian prion diseases identifies dynamic gene signatures shared between species [human_scRNAseq]

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Single-cell transcriptomics of mammalian prion diseases identifies dynamic gene signatures shared between species [human_bulkRNAseq]

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Transcriptional signature of prion-induced neurotoxicity in a Drosophila model of transmissible mammalian prion disease

Project description:Prion diseases are fatal transmissible neurodegenerative conditions of humans and animals that arise through neurotoxicity induced by PrP misfolding. The cellular and molecular mechanisms of prion-induced neurotoxicity remain undefined. Understanding these processes will underpin therapeutic and control strategies for human and animal prion diseases, respectively. Prion diseases are difficult to study in their natural hosts and require the use of tractable animal models. Here we used RNA-Seq-based transcriptome analysis of prion-exposed Drosophila to probe the mechanism of prion-induced neurotoxicity. Adult Drosophila transgenic for pan neuronal expression of ovine PrP targeted to the plasma membrane exhibit a neurotoxic phenotype evidenced by decreased locomotor activity after exposure to ovine prions at the larval stage. Pathway analysis and quantitative PCR of genes differentially expressed in prion-infected Drosophila revealed up-regulation of cell cycle activity and DNA damage response, followed by down-regulation of eIF2 and mTOR signalling. Mitochondrial dysfunction was identified as the principal toxicity pathway in prion-exposed PrP transgenic Drosophila. The transcriptomic changes we observed were specific to PrP targeted to the plasma membrane since these prion-induced gene expression changes were not evident in similarly-treated Drosophila transgenic for cytosolic pan neuronal PrP expression, or in non-transgenic control flies. Collectively, our data indicate that aberrant cell cycle activity, repression of protein synthesis and altered mitochondrial function are key events involved in prion-induced neurotoxicity, and correlate with those identified in mammalian hosts undergoing prion disease. These studies highlight the use of PrP transgenic Drosophila as a genetically well-defined tractable host to study mammalian prion biology.

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Transcriptional signature of prion-induced neurotoxicity in a Drosophila model of transmissible mammalian prion disease

Project description:Transcriptional signature of prion-induced neurotoxicity in a Drosophila model of transmissible mammalian prion disease

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Skeletal-Muscle Glutamate-Ammonia Ligase as Potential Biomarker of Preclinical Prion Diseases

Project description:Skeletal-Muscle Glutamate-Ammonia Ligase as Potential Biomarker of Preclinical Prion Diseases

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Skeletal-Muscle Glutamate-Ammonia Ligase as Potential Biomarker of Preclinical Prion Diseases

Project description:We provide here a comprehensive transcriptional profiling of murine blood, spleen and skeletal muscle and brain on eight different time points after intracerebral prion inoculation. Our findings provide a detailed time course of extra-neural, transcriptional changes during prion disease which we presume to be of immediate relevance for biomarker development. Data analysis scripts can be found on https://github.com/marusakod/RML_extraneural_organs.

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Gene expression differences between prion-resistant and prion-susceptible cells

Project description:Prions consist of aggregates of abnormal conformers of cellular prion protein (PrPC). They propagate by recruiting host-encoded PrPC although the critical interacting proteins and the reasons for the differences in susceptibility of distinct cell lines and populations are unknown. We derived a lineage of cell lines with markedly differing susceptibilities, unexplained by PrPC expression differences, to identify such factors. We examined the transcriptomes of prion-resistant revertants, isolated from highly susceptible cells, and identified a gene expression signature associated with susceptibility. Several of these genes encode proteins with a role in extracellular matrix (ECM) remodelling, a compartment in which disease-related PrP deposits. Loss-of-function of nine of these genes significantly increased susceptibility. Remarkably, inhibition of fibronectin 1 binding to integrin α8 by RGD peptide inhibited metalloproteinases (MMP)-2/9 whilst increasing prion propagation rates. This indicates that prion replication may be controlled by MMPs at the ECM in an integrin-dependent manner.

2014-07-31 | GSE56275 | GEO

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