Figure 7.

A schematic model for the molecular mechanism of chlorosis. Inducible silencing of the HSP90C gene causes a reduction of HSP90C levels in the chloroplast, which causes the loss of protein homeostasis in the chloroplast. The disruption of protein homeostasis leads chloroplasts to produce ROS in a light-dependent manner. The effects of ROS and SA are enhanced by a self-amplifying loop. ROS serves as the chloroplast retrograde signal and activates other retrograde signaling pathways, leading to the upregulation of pathogenesis-related (PR) genes and the downregulation of chloroplast- and photosynthesis-related genes (CPRGs). Reduced supply of HSP90C in the chloroplast induces the activation of the ER stress response and the upregulation of JA/ET/ABA pathway genes, likely through SA, ROS, or other signaling pathways. ROS, SA, the activation of PR genes, and other stress responses including JA/ET/ABA pathways could stimulate the cell death pathway. The downregulation of CPRGs may be the primary cause of chlorosis, and ROS-mediated triggering of HR-like cell death in the chlorotic tissues could have a role in the development of chlorosis. Solid line arrows indicate the steps with experimental support, whereas broken line arrows are hypothetical.