The increase in environmental temperature due to global warming is a critical threat to plant growth and productivity. Heat stress can cause impairment in several biochemical and physiological processes. Plants sense and respond to this adverse environmental condition by activating a plethora of defense systems. Among them, the heat stress response (HSR) involves an intricate network of heat shock factors (HSFs) and heat shock proteins (HSPs). However, a growing amount of evidence suggests that reactive oxygen species (ROS), besides potentially being responsible for cellular oxidative damage, can act as signal molecules in HSR, leading to adaptative responses. The role of ROS as toxic or signal molecules depends on the fine balance between their production and scavenging. Enzymatic and non-enzymatic antioxidants represent the first line of defense against oxidative damage and their activity is critical to maintaining an optimal redox environment. However, the HS-dependent ROS burst temporarily oxidizes the cellular environment, triggering redox-dependent signaling cascades. This review provides an overview of the redox-activated mechanisms that participate in the HSR.
Heat stress (HS) severely affects different cellular compartments operating in metabolic processes and represents a critical threat to plant growth and yield. Chloroplasts are crucial for heat stress response (HSR), signaling to the nucleus the environmental challenge and adjusting metabolic and biosynthetic functions accordingly. GENOMES UNCOUPLED 1 (GUN1), a chloroplast-localized protein, has been recognized as one of the main players of chloroplast retrograde signaling. Here, we investigate HSR in Arabidopsis wild-type and gun1 plantlets subjected to 2 hours of HS at 45°C. In wild-type plants, Reactive Oxygen Species (ROS) accumulate promptly after HS, contributing to transiently oxidize the cellular environment and acting as signaling molecules. After 3 hours of physiological recovery at growth temperature (22°C), the induction of enzymatic and non-enzymatic antioxidants prevents oxidative damage. On the other hand, gun1 mutants fail to induce the oxidative burst immediately after HS and accumulate ROS and oxidative damage after 3 hours of recovery at 22°C, thus resulting in enhanced sensitivity to HS. These data suggest that GUN1 is required to oxidize the cellular environment, participating in the acquisition of basal thermotolerance through the redox-dependent plastid-to-nucleus communication.
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