Figure 6. Mechanistic view about the conversion of caspases from tumor suppressors to tumors promoters in scrib Ras^V12 mutant cells.

(A) After scrib^−/− mutant cells have formed in mosaic discs, a cell competition signal mediated by Eiger triggers JNK and caspase activity which induces apoptosis of scrib mutant cells (dashed outline of the cell). (B) After scrib^−/− Ras^V12 cells have formed, JNK activity may be induced by the same cell competition signal as in scrib^−/− mutant cells (early). However, despite activation of JNK and caspases in scrib Ras^V12 cells, Ras^V12 keeps these cells in an ‘undead’-like condition and enables caspases to initiate a feedback amplification loop involving ROS generation and recruitment of hemocytes which amplifies JNK and caspase activity (late). This amplification loop is necessary for malignant growth and invasion. Neighboring wild-type cells undergo apoptosis (dashed outline of the cell). The mechanism of non-autonomous apoptosis is not clear.