Figure 1.

Activation of apoptosis through p53 and rpr-associated pathways. Apoptosis is primarily initiated through either p53 or Jun-induced (JNK) transcriptional activation of the Inhibitor of Apoptosis (IAP, in Drosophila Diap) inhibitors hid, rpr and grim. While p53 is primarily activated by DNA damage and disruption of the cell cycle, JNK signaling is activated downstream of cellular stress, such as endoplasmic reticulum (ER) stress, through Ire1 and Cdk5. ER stress occurs when misfolding proteins, like the rhodopsin mutant Rh1^G69D, accumulate in the ER (Chow et al. 2016). Expression of rpr, grim, and hid leads to inhibition of Diap1, releasing the inhibition on initiator caspases and allows for the activation of effector caspases and downstream apoptosis. Models used in this or previous studies of retinal degeneration in the DGRP are indicated in white.