Increases in ambient temperatures have been a severe threat to crop production in many countries around the world under climate change. Chloroplasts serve as metabolic centers and play a key role in physiological adaptive processes to heat stress. In addition to expressing heat shock proteins that protect proteins from heat-induced damage, metabolic reprogramming occurs during adaptive physiological processes in chloroplasts. Heat stress leads to inhibition of plant photosynthetic activity by damaging key components functioning in a variety of metabolic processes, with concomitant reductions in biomass production and crop yield. In this review article, we will focus on events through extensive and transient metabolic reprogramming in response to heat stress, which included chlorophyll breakdown, generation of reactive oxygen species (ROS), antioxidant defense, protein turnover, and metabolic alterations with carbon assimilation. Such diverse metabolic reprogramming in chloroplasts is required for systemic acquired acclimation to heat stress in plants.

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Inositol-requiring enzyme 1 (IRE1) is the most conserved transducer of the unfolded protein response that produces either adaptive or death signals depending on the amplitude and duration of its activation. Here, we report that SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE 6 (SPL6)-deficient plants displayed hyperactivation of the endoplasmic reticulum (ER) stress sensor IRE1, leading to cell death in rice panicles, indicating that SPL6 is an essential survival factor for the suppression of persistent or intense ER stress conditions. Importantly, knockdown of the hyperactivated mRNA level of IRE1 rescues panicle apical abortion in the spl6-1 transgenic plants harbouring the IRE1-RNAi constructs, establishing the genetic linkage between the hyperactivation of IRE1 and cell death in spl6-1. Our findings reveal a novel cell survival machinery in which SPL6 represses the transcriptional activation of the ER stress sensor IRE1 in control of ER stress signalling outputs that hinge on a balance between adaptive and death signals for determining cell fates during ER stress.