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. 2019 Mar 25;10(4):288. doi: 10.1038/s41419-019-1496-2

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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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Fig. 2 — a RNAi-mediated suppression of dMfn results in mitochondrial fragmentation. Confocal analysis of mitoGFP in the larval mechanosensory axons. The quantification of mitochondrial length is shown as a combined violin and box plot (p value, two-tailed unpaired t-test compared to control). b The knockdown of dMfn causes defects in mitochondrial cristae. Ultrastructural analysis of the brains in adult dMfn RNAi flies (m, mitochondria; nu, cell nuclei). Asterisks, chi-square two-tailed, 95% confidence intervals. c The knockdown of dMfn does not affect overall mitochondrial mass. Mitochondrial mass was assessed by measuring the activity of the mitochondrial matrix enzyme citrate synthase in adults (ns, p > 0.05, two-tailed unpaired t-test compared to control). d The knockdown of dMfn causes a loss of ATP in adult flies (mean ± SD, asterisks, two-tailed unpaired t-test compared to control). Genotypes in a Control: w; elavGal4/+; UASmitoGFP/+, dMfn RNAi: w; elavGal4/dMfn RNAi; UASmitoGFP/+. b–d Control: w; +; daGal4/+, dMfn RNAi: w; dMfn RNAi/+; daGal4/+