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Abstract:
Plants can be primed to withstand otherwise lethal heat stress (HS) through exposure to a foregoing temporary and mild HS, commonly known as the ´thermopriming stimulus´. Plants can also generate memories of a previous stress encounter and reset their physiology to the original cellular state once the stress has vanished. The priming stimulus triggers a widespread change of transcripts, proteins, and metabolites, which is crucial for maintaining the memory state but may not be required for growth and development under optimal conditions or may even be hurtful. In such a scenario, recycling mechanisms such as autophagy are crucial for re-establishing cellular homeostasis and optimizing resource use for post-stress growth. While pivotal for eliminating heat-induced protein aggregates and protecting plants from the harmful impact of HS, recent evidence implies that autophagy also breaks down heat-induced protective macromolecules, including heat shock proteins, functioning as a resetting mechanism during the recovery from mild HS. This review provides an overview of the latest advances in understanding the multifaceted functions of autophagy in the context of HS, with a specific emphasis on its roles in recovery from mild HS, and the modulation of HS memory.
