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. 2020 Mar 10;10:4401. doi: 10.1038/s41598-020-61244-3

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© The Author(s) 2020

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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The effect of complex I downregulation on apoptosis, proliferation and tissue growth is mediated by Tor. (A) Induction of apoptosis (Dcp1) and proliferation (p-H3) after ND-49-RNAi in the posterior domain (right half) of the wing disc is rescued by TOR-RNAi. (B) Overexpression of Tor in the posterior domain leads to the same phenotype as ND-49-RNAi. (C) Quantifications of apoptosis (Dcp1), (D) the relative mitotic index (p-H3) and (E) the size of posterior wing disc compartment after ND-49-RNAi, Tor-RNAi and Tor overexpression. We detect interaction with the effect of ND-49 knockdown using ANOVA [***p < 0.001; *p < 0.05]. LacZ represents control. (F) Graphical summary of Fig. 2.