FIGURE 4.

Non-autonomous JNK signalling. The activation of JNK signalling in one group of cells can have non-autonomous effects on the growth and proliferation of their neighbours, due to the upregulation of various signalling pathway initiators. (A) The generation of “undead” cells via the upregulation of p35 while simultaneously inducing apoptosis via Diap1 mutation or X-ray application leads to JNK signalling activation, the expression and secretion of Wg and Dpp ligands, and the survival and overproliferation of neighbouring cells due to Wg and TGF-β signalling pathway activation. (B) The upregulation of JNK signalling that occurs in scrib^–/– cells leads to expression and secretion of the Upd-family ligands, which can activate Jak-STAT signalling in neighbouring Ras85D^V12-expressing tumourigenic cells, leading to their survival and overproliferation, and possibly their invasiveness. (C) Cells expressing Ras85D^V12 coupled with mitochondrial gene mutations upregulate JNK signalling, due to p53 and ROS activity. Said JNK signalling downregulates SWH signalling, derepressing Yki, and also upregulates expression and secretion of Wg and the Upd-family ligands, activating Jak-STAT and Wg signalling in neighbouring cells and promoting their survival and overproliferation. Gene and protein name abbreviations used in the diagram are as follows: Death-associated inhibitor of apoptosis 1 (Diap1), decapentaplegic (dpp), wingless (wg), unpaired 1 (upd1), unpaired 2 (upd2), unpaired 3 (upd3), Yorkie (Yki).