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. 2019 Dec 10;9:18666. doi: 10.1038/s41598-019-53508-4

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Loss of Sod1 function impairs motor behaviour in Gem3 mutant flies. Placed in a Gem3^BART genetic background, heterozygotes for an enzymatic null Sod1 allele (+/Sod1^G51S) only induce deficits in old age (left panel). A similar outcome is achieved in Gem3^BART flies with muscle-selective RNAi-mediated knockdown of Sod1 (middle panel). The use of a stronger RNAi transgene causes defects at an earlier stage of adult life (right panel). Data presented are the mean ± S.E.M. of at least 4 independent experiments, and, for each time point measured, n ≥ 60 males (♂) per genotype. Significance as tested by two-way ANOVA, followed by Bonferroni’s post hoc tests, is indicated by the exact p-value.