Figure 8.

Control of autophagy by ER stress and ER-derived ROS in C. reinhardtii. Tunicamycin (tun) treatment results in toxic accumulation of unfolded proteins in the ER, leading to autophagy activation as a defensive mechanism. ER stress also increases ROS production in the ER by de oxidoreductase ERO1, which contributes to the up-regulation of autophagy. The antioxidant properties of GSH counterbalance ROS signaling to the autophagic machinery but do not abrogate ER stress, resulting in partial inactivation of autophagy.