Figure 7

Model of tissue homeostasis maintenance after an ER stress. Chronic ER stress activates the PERK pathway, which results in ATF4 expression. ATF4 has two antagonistic functions. On one hand, ATF4 induces a caspase-dependent apoptosis by repressing diap1 expression. On the other hand, it favors tissue homeostasis through the induction of dilp8 expression by Rac1/Slpr/JNK pathway activation. The role of Msn in the control of the observed developmental delay remains to be elucidated. It could either negatively regulate the JNK pathway or have a JNK pathway-independent mechanism of action