Tissue-specific requirement for G9a in OS response.

Kaplan-Meier survival curves comparing G9a-knockdown flies to controls. Knockdown was targeted to (A) fat body and (B) dilp2-expressing cells. (A) Survival curves of flies with fat body–specific G9a knockdown (lsp2-Gal4 + UAS-G9a-RNAi) and controls (lsp2-Gal4) (median survival time: lsp2-Gal4 + UAS-G9a-RNAi, 15 h, n = 46 versus lsp2-Gal4, 23 h, n = 46; p = 0.0007). (B) Survival curves of flies with insulin-secreting cell-specific G9a knockdown (dilp2-Gal4 + UAS-G9a-RNAi) and controls (dilp2-Gal4) (median survival time: dilp2-Gal4 + UAS-G9a-RNAi, 22 h, n = 41 versus dilp2-Gal4, 33 h, n = 45; p = 0.0002). Fat body–or insulin-secreting cell–specific drivers were combined with a UAS-G9a RNAi construct (lsp2-Gal4 + UAS-G9a-RNAi [A], dilp2-Gal4 + UAS-G9a RNAi [B]) to repress G9a expression in a tissue/cell-specific manner or crossed to the isogenic background of the RNAi lines to generate the isogenic controls. Survival curves showing percent survival and SE over time were plotted using Graphpad, and p-values were obtained using the Gehan-Breslow-Wilcoxon test. All experiments were independently replicated at least three times. The numerical data depicted in this figure can be found in S5 Data. OS, oxidative stress; RNAi, RNA interference; SE, standard error.