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Bar-coding neurodegeneration: identifying subcellular effects of human neurodegenerative disease proteins using Drosophila leg neurons
Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.ORCID iD: 0000-0001-5095-541X
2017 (English)In: Disease Models and Mechanisms, ISSN 1754-8403, E-ISSN 1754-8411, Vol. 10, no 8, p. 1027-1038Article in journal (Refereed) Published
Abstract [en]

Genetic, biochemical and histological studies have identified a number of different proteins as key drivers of human neurodegenerative diseases. Although different proteins are typically involved in different diseases, there is also considerable overlap. Addressing disease protein dysfunction in an in vivo neuronal context is often time consuming and requires labor-intensive analysis of transgenic models. To facilitate the rapid, cellular analysis of disease protein dysfunction, we have developed a fruit fly (Drosophila melanogaster) adult leg neuron assay. We tested the robustness of 41 transgenic fluorescent reporters and identified a number that were readily detected in the legs and could report on different cellular events. To test these reporters, we expressed a number of human proteins involved in neurodegenerative disease, in both their mutated and wild-type versions, to address the effects on reporter expression and localization. We observed strikingly different effects of the different disease proteins upon the various reporters with, for example, A beta(1-42) being highly neurotoxic, tau, parkin and HTT128Q affecting mitochondrial distribution, integrity or both, and A beta(1-42), tau, HTT128Q and ATX1(82Q) affecting the F-actin network. This study provides proof of concept for using the Drosophila adult leg for inexpensive and rapid analysis of cellular effects of neurodegenerative disease proteins in mature neurons.

Place, publisher, year, edition, pages
COMPANY OF BIOLOGISTS LTD , 2017. Vol. 10, no 8, p. 1027-1038
Keywords [en]
Neurodegeneration; Protein toxicity; Cellular effects; Axon transport; Apoptosis
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
URN: urn:nbn:se:liu:diva-139907DOI: 10.1242/dmm.029637ISI: 000406796600009PubMedID: 28615189OAI: oai:DiVA.org:liu-139907DiVA, id: diva2:1135752
Note

Funding Agencies|King Gustaf V and Queen Victorias Freemasons Foundation (Svenska Frimurarorden) [700-0557]

Available from: 2017-08-24 Created: 2017-08-24 Last updated: 2017-09-13

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Fernius, JosefinStarkenberg, AnnikaThor, Stefan
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