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. 2018 Nov 7;9:4675. doi: 10.1038/s41467-018-07114-z

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© The Author(s) 2018

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. 3 — AdoR acts upstream of TNF^Egr during chronic polarity stress. a, b Activation of TRE-dsRed in sal> ent2, AdoR or in sal> scrib-Ri, AdoR discs is suppressed by expression of AdoR-RNAi, mutation in TNF^egr, expression of TNFR^grnd-RNAi or expression of TNF^egr-RNAi. c–g Mild activation of TRE-dsRed caused by overexpression of AdoR alone is rescued by AdoR-RNAi, in a TNF^egr mutant background, by TNFR^grnd-RNAi or by TNF^egr-RNAi. h–j TRE-dsRed activation triggered by overexpression of TNF^Egr is suppressed by JNK^bsk-RNAi or TNFR^grnd-RNAi but is not affected by AdoR-RNAi. This experiment was carried out at 29 °C. Scale bars, 50 μm. In graphs, means are shown, and error bars represent ±SD; ****P < 0.0001, ^n.s.P ≥ 0.05, unpaired two-tailed Student’s t-test (males and females pooled together)