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. 2017 Aug 16;8:265. doi: 10.1038/s41467-017-00334-9

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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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Fig. 2 — Pheromone production after infection with immune and metabolic mutants. a, b Pheromone (here and thereafter methyl palmitate shown as example) production of CantonS or OregonR wild-type flies, and flies deficient in the Imd immune response pathway (RelE20 and IMD¹⁵⁶) with Pseudomonas entomophila infection (green) and without (white; a), or of flies, where the IMD (Imd flies) or the Toll (Toll flies and spz* flies) response pathway were artificially activated (b). c Pheromone production after infection with live (green) or heat-killed (gray) bacteria. d GC-MS profiles of live bacteria, heat-killed bacteria, and mock-infected control flies. e Pheromone production of flies with either decreased juvenile hormone (Aug21-gal4 x UAS-DTI flies), insulin metabolism (FOXO flies), or stress responses (p38a flies) and their parental control lines. RNAi lines tested at the non-active 25 °C served as further controls. f Pheromone production of flies with or without artificial activation of Rheb (an inhibitor of the FOXO pathway) with infection (green) or without (white)