TY - JOUR T1 - High JNK following Ras/Rpr/Tak1 over-expression in imaginal discs of <em>Drosophila</em> reduces post-pupariation ecdysone via Dilp8 resulting in early pupal death JF - bioRxiv DO - 10.1101/049882 SP - 049882 AU - Mukulika Ray AU - Subhash C. Lakhotia Y1 - 2018/01/01 UR - http://biorxiv.org/content/early/2018/07/13/049882.abstract N2 - We examined reasons for early pupal death following expression of certain transgenes with predominantly eye- (GMR-GAL4 or sev-GAL4) or wing- (MS1096-GAL4) disc specific drivers. The GMR-GAL4&gt;UAS-Ras1V12 expression or co-expression of sev-GAL4&gt;UAS-Ras1V12 and UAS-hsrω-RNAi transgene or EP3037 to down or up-regulate, respectively, the hsrω lncRNAs caused early (~25–30 Hr after pupa formation, APF) pupal death, with absence of the normal 8–12 Hr APF ecdysone surge. Exogenous ecdysone between 8–20 Hr APF partially suppressed the early death. Similar early pupal death was also seen following GMR-GAL4&gt;driven UAS-tak1 expression or MS1096-GAL4 driven Ras/JNK activation. Genotypes showing early pupal death displayed increase in some JNK pathway members, and Dilp8 in late larval and more so in early pupal eye discs, reduced transcripts of ptth in brain lobes and of ecdysone biosynthesis enzymes in prothoracic glands of 8–9 Hr old pupae. High JNK activity in late larval imaginal discs triggers greater Dilp8 secretion from them soon after pupa formation, which inhibits post-pupal ecdysone synthesis in prothoracic gland, leading to early pupal death. This highlights how mis-regulated signaling in one tissue can have global deleterious consequences through downstream events in other tissues, reemphasizing roles of inter-organ signaling in life of an organism. ER -