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. 2017 Sep 12;7:11317. doi: 10.1038/s41598-017-10550-4

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© The Author(s) 2017

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 cell death induced by suppressing Hh signalling is JNK-independent. (A) Ectopic JNK signalling activity can be revealed by using a puc-lacZ. In a positive control experiment, puc-lacZ reporter (red) is activated when Dpp signalling is suppressed by expressing dad within the nub-Gal4 domain. (B,C) Suppression of Hh signalling by expressing smo-RNAi does not induce ectopic puc-lacZ (red). (D–I) Inhibition of JNK signalling by expressing a dominant negative form of bsk ^DN (E and G) or by suppressing an upstream effector (by expressing hep-RNAi) (I) can not rescue the apoptosis induced by expressing smo-RNAi. (D,F and H) The control experiments show no apoptosis when bsk ^DN or hep-RNAi is expressed alone. (J) Statistics for the apoptotic cell number per wing disc of each genotype mentioned above. ns stands for no significant difference.