Besides providing energy to sustain life, mitochondria also play crucial roles in stress response and programmed cell death. The mitochondrial hallmark lipid, cardiolipin (CL), is essential to the maintenance of mitochondrial structure and function. However, how mitochondria and CL are involved in stress response is not as well defined in plants as in animal and yeast cells. We previously revealed a role for CL in mitochondrial fission and in heat stress response in Arabidopsis . To further determine the involvement of mitochondria and CL in plant heat response, here we treated Arabidopsis seedlings with varied lengths of acute heat stress. These treatments resulted in decreases in mitochondrial membrane potential, disruption of mitochondrial ultrastructure, accumulation of mitochondrial reactive-oxygen species (ROS), and redistribution of CL to the outer mitochondrial membrane and to a novel type of vesicle. The level of the observed changes correlated with the severeness of the heat stress, indicating the strong relevance of these processes to stress response. Our findings provide the basis for studying mechanisms underpinning the role of mitochondria and CL in plant stress response.
Keyphrases
- heat stress
- reactive oxygen species
- oxidative stress
- heat shock
- cell death
- transcription factor
- cell wall
- induced apoptosis
- intensive care unit
- endoplasmic reticulum
- risk assessment
- single cell
- dna damage
- signaling pathway
- climate change
- human health
- fatty acid
- extracorporeal membrane oxygenation
- mechanical ventilation