FIGURE 2.

The chloroplast and mitochondrion are involved in the response to heat stress in plants. Except the PM, the other key sites of ROS generation are PSII in chloroplasts and complex I/III in mitochondria. Heat affects the fluidity of the thylakoid membrane, and unsaturated lipids near the QB site are particularly vulnerable to peroxidation. The lipid peroxidation products affect the stability of photosystem proteins; the electron transport chain is restrained, and ¹O₂ forms on the electron acceptor side and ^•OH on the electron donor side. High temperatures trigger the chloroplast UPR and retrograde signaling pathway. Similarly, heat stress causes CL lipid peroxidation in the mitochondrion membrane, which inhibits the activity of CCO; but membrane depolarization via CCCP can inhibit ROS generation. The electron transport suppressed in the respiratory chain induces the production of ROS, which triggers both the mitochondrial UPR and retrograde signaling pathway.