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Detection of Aggregation-Competent Tau in Neuron-Derived Extracellular Vesicles
Open AccessArticle

Vesicular Axonal Transport is Modified In Vivo by Tau Deletion or Overexpression in Drosophila

Author to whom correspondence should be addressed.
Institut de Génomique Fonctionnelle (IGF), Université de Montpellier, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM), 34094 Montpellier, France
Current address: SANOFI-Algeria, 29, 30, 31 Micro Zone d’activités, Bâtiment B Hydra, 16035 Alger, Algérie.
Current address: Department of Physiology, University of Lausanne, 1005 Lausanne, Switzerland.
Int. J. Mol. Sci. 2018, 19(3), 744;
Received: 30 January 2018 / Revised: 23 February 2018 / Accepted: 2 March 2018 / Published: 6 March 2018
(This article belongs to the Special Issue Tau Function and Dysfunctional Tauopathies)
Structural microtubule associated protein Tau is found in high amount in axons and is involved in several neurodegenerative diseases. Although many studies have highlighted the toxicity of an excess of Tau in neurons, the in vivo understanding of the endogenous role of Tau in axon morphology and physiology is poor. Indeed, knock-out mice display no strong cytoskeleton or axonal transport phenotype, probably because of some important functional redundancy with other microtubule-associated proteins (MAPs). Here, we took advantage of the model organism Drosophila, which genome contains only one homologue of the Tau/MAP2/MAP4 family to decipher (endogenous) Tau functions. We found that Tau depletion leads to a decrease in microtubule number and microtubule density within axons, while Tau excess leads to the opposite phenotypes. Analysis of vesicular transport in tau mutants showed altered mobility of vesicles, but no change in the total amount of putatively mobile vesicles, whereas both aspects were affected when Tau was overexpressed. In conclusion, we show that loss of Tau in tau mutants not only leads to a decrease in axonal microtubule density, but also impairs axonal vesicular transport, albeit to a lesser extent compared to the effects of an excess of Tau. View Full-Text
Keywords: microtubule; axonal transport; tauopathy; Alzheimer’s disease microtubule; axonal transport; tauopathy; Alzheimer’s disease
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MDPI and ACS Style

Talmat-Amar, Y.; Arribat, Y.; Parmentier, M.-L. Vesicular Axonal Transport is Modified In Vivo by Tau Deletion or Overexpression in Drosophila. Int. J. Mol. Sci. 2018, 19, 744.

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