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Endogenous Tau deletion affects sex-dependent outcome to traumatic brain injury in Drosophila

ABSTRACT: Endogenous Tau deletion affects sex-dependent outcome to traumatic brain injury in Drosophila

PROVIDER: PRJNA626587 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11574137.fastq.gz	Fastqsanger.gz
	SRR11574138.fastq.gz	Fastqsanger.gz
	SRR11574139.fastq.gz	Fastqsanger.gz
	SRR11574140.fastq.gz	Fastqsanger.gz
	SRR11574141.fastq.gz	Fastqsanger.gz

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Endogenous Tau deletion affects sex-dependent outcome to traumatic brain injury in Drosophila

Project description:Adult male and female Tau-KO flies were inflicted with traumatic brain injury using high-impact trauma device. Brains were dissected at control, 1, 2 and 4 hours post-TBI. Total RNA was extracted from fly brains and 3'mRNA-seq was performed to assess gene expression changes in response to TBI in both sexes. 3 replicates were sequenced for each condition.

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Project description:Tau (MAPT) is a microtubule-associated protein causing frequent neurodegenerative diseases or inherited frontotemporal lobar degenerations. Emerging evidence for non-canonical functions of Tau in DNA protection and P53 regulation suggests its involvement in cancer. Indeed, Tau expression correlates with cancer-specific survival or response to microtubule therapeutics. These data may imply common molecular pathways involved in the pathogenesis of neurodegenerative disorders and cancer. To bring new evidence that Tau represents a key protein in cancer, we present an in silico pan-cancer analysis of MAPT transcriptomic profile in over 11000 clinical samples and over 1300 pre-clinical samples provided by the TCGA and the DEPMAP datasets respectively. We completed this analysis by exploring a possible interplay of MAPT with wild-type or mutated P53. Then, we calculated the impact of MAPT expression on clinical outcome and drug response. Overall, the results support a relevant role of the MAPT gene in several cancer types, although the contribution of Tau to cancer appears to very much depend on the cellular context.

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Recapitulation of endogenous 4R tau expression and formation of insoluble tau in directly reprogrammed human neurons

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Project description:Traumatic brain injury (TBI) increases one’s risk of developing Alzheimer’s disease and tauopathy. Yet, the mechanisms linking TBI to neurodegenerative disease remain poorly defined. Mounting recent evidence indicates that defects in brain lymphatic drainage contribute to multiple neurodegenerative diseases. Here, we investigated whether promoting brain lymphatic drainage recuperation following TBI via treatment with the lymphangiogenic factor VEGFC mitigates the ability of TBI to exacerbate tauopathy. In this study, we show that a single mild TBI leads to worsened neuropathology, brain macrophage activation, and neurodegeneration in the PS19 mouse model of tauopathy. Moreover, we find that viral vector-based delivery of VEGFC into the meningeal compartment 24 hours post-TBI ameliorates tau-mediated neurodegenerative disease pathogenesis. Findings from these studies offer new insights into how TBI leads to the development of tauopathy later in life and suggest that VEGFC-based treatments might offer a therapeutic strategy to limit tauopathy after sustaining a head injury.

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