Effects on Dopaminergic Neurons Are Secondary in COX-Deficient Locomotor Dysfunction in Drosophila

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Yalgin , C , Rovenko , B , Andjelkovic , A , Neefjes , M , Oymak , B , Dufour , E , Hietakangas , V & Jacobs , H T 2020 , ' Effects on Dopaminergic Neurons Are Secondary in COX-Deficient Locomotor Dysfunction in Drosophila ' , iScience , vol. 23 , no. 8 , 101362 . https://doi.org/10.1016/j.isci.2020.101362

Title: Effects on Dopaminergic Neurons Are Secondary in COX-Deficient Locomotor Dysfunction in Drosophila
Author: Yalgin, Cagri; Rovenko, Bohdana; Andjelkovic, Ana; Neefjes, Margot; Oymak, Burak; Dufour, Eric; Hietakangas, Ville; Jacobs, Howard T.
Contributor: University of Helsinki, Centre of Excellence in Stem Cell Metabolism
University of Helsinki, Institute of Biotechnology
University of Helsinki, Molecular and Integrative Biosciences Research Programme
Date: 2020-08-21
Language: eng
Number of pages: 75
Belongs to series: iScience
ISSN: 2589-0042
URI: http://hdl.handle.net/10138/319506
Abstract: Dopaminergic (DA) neurons have been implicated as key targets in neurological disorders, notably those involving locomotor impairment, and are considered to be highly vulnerable to mitochondrial dysfunction, a common feature of such diseases. Here we investigated a Drosophila model of locomotor disorders in which functional impairment is brought about by pan-neuronal RNAi knockdown of subunit COX7A of cytochrome oxidase (COX). Despite minimal neuronal loss by apoptosis, the expression and activity of tyrosine hydroxylase was decreased by half. Surprisingly, COX7A knockdown specifically targeted to DA neurons did not produce locomotor defect. Instead, using various drivers, we found that COX7A knockdown in specific groups of cholinergic and glutamatergic neurons underlay the phenotype. Based on our main finding, the vulnerability of DA neurons to mitochondrial dysfunction as a cause of impaired locomotion in other organisms, including mammals, warrants detailed investigation.
Subject: MITOCHONDRIAL-DNA DELETIONS
TARGETED GENE-EXPRESSION
ALTERNATIVE-OXIDASE
PROTEIN
NEURODEGENERATION
INACTIVATION
REPORTER
PATHWAY
MARKER
MODEL
1184 Genetics, developmental biology, physiology
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