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Skeletal muscle gene expression from P301L tau expressing mice using NanoString

ABSTRACT: Skeletal muscle gene expression from P301L tau expressing mice using NanoString

PROVIDER: PRJNA1042653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26875200_1.fastq.gz	Fastqsanger.gz
	SRR26875200_2.fastq.gz	Fastqsanger.gz
	SRR26875201_1.fastq.gz	Fastqsanger.gz
	SRR26875201_2.fastq.gz	Fastqsanger.gz
	SRR26875202_1.fastq.gz	Fastqsanger.gz

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Skeletal muscle gene expression from P301L tau expressing mice using NanoString

Project description:We analyzed gene expression in regions from tibialis anterior cross sections of P301L tau expressing mice and controls. The regions were: standard myofibers, regions containing centrally nucleated myofibers, myofibers proximal to nerve bundle, and myofibers proximal to vasculature

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Project description:Utilizing non-human primates to study the role of human Tau and its related pathologies is logical and important due to their closer similarity to human brain structure and function. In our earlier research, we generated a transgenic cynomolgus monkey model expressing Tau (P301L) through lentiviral infection of monkey embryos. These monkeys exhibited age-dependent neurodegeneration and motor dysfunction. Single-cell RNA sequencing (scRNA-seq) is a powerful and promising technique for elucidating the cellular complexity and pathology across different tissues. However, single-cell data from non-human primate models of Tau pathology are currently nonexistent. In this study, we performed single-nuclei RNA sequencing (snRNA-seq) on the hippocampus, striatum, and spinal cord of Tau (P301L) monkey, providing the first single-cell atlas of multiple tissue regions in a non-human primate model that simulates human tauopathies. This will offer crucial data references for cross-species single-cell level studies of tau and its related pathologies.

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Project description:Alzheimer’s disease (AD) is the most prevalent form of neurodegeneration. Despite the well-established link between tau aggregation and clinical progression, the major pathways driven by this protein to intrinsically damage neurons are incompletely understood. To model AD-relevant neurodegeneration driven by tau, we overexpressed non-mutated human tau in primary mouse neurons and observed substantial axonal degeneration and cell death, a process accompanied by activated caspase 3. Mechanistically, we detected deformation of the nuclear envelope and increased DNA damage response in tau-expressing neurons. Gene profiling analysis further revealed significant alterations in the mitogen-activated protein kinase (MAPK) pathway; moreover, inhibitors of dual leucine zipper kinase (DLK) and c-Jun N-terminal kinase (JNK) were effective in alleviating wild-type human tau-induced neurodegeneration. In contrast, mutant P301L human tau was less toxic to neurons, despite causing comparable DNA damage. Axonal DLK activation induced by wild-type tau potentiated the impact of DNA damage response, resulting in overt neurotoxicity. In summary, we have established a cellular tauopathy model highly relevant to AD and identified a functional synergy between the MAPK-DLK axis and DNA damage response in the neuronal degenerative process.

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