Abstract - Plants are able to survive normally lethal temperatures if first acclimated by a more moderate heat stress, a process that can occur on a daily basis. We have dissected mechanisms involved in high temperature acclimation using both genetics and biochemistry in Arabidopsis. Mutants (“hot mutants”) unable to acclimate have identified protein folding, ability to control reactive nitrogen species and ability to recover translation as critical to acclimation. The HOT1 gene encodes the molecular chaperone Hsp101, which is an AAA protein that uses the power of ATP to disaggregate proteins damaged by heat stress. Specific proteins remain insoluble after heat stress in the hot1 mutant, consistent with the Hsp101 activity. We also carried out a suppressor screen of a dominant negative allele of hot1 in order to identify factors that interact with HSP101 or that are involved in thermotolerance. One suppressor, shot1 (for suppressor of hot1), encodes a mitochondrial transcription termination factor (mTERF)–related protein, one of 35 Arabidopsis mTERFs about which there is limited functional data. Reduced heat-induced oxidative damage is the likely cause of shot1 thermotolerance, indicating HSP101 repairs protein oxidative damage and/or reduced oxidative damage allows recovery in the absence of HSP101. The heat tolerance of shot1 emphasizes the importance of mitochondria in stress tolerance, and defining its function may provide insights into control of oxidative damage for engineering stress-resistant plants.

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