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Impact of mitochondrial respiration efficiency on plant cell metabolism

Final Report Summary - RESPARA (Impact of mitochondrial respiration efficiency on plant cell metabolism)

Respiration is an essential cellular metabolic pathway that provides energy to fuel housekeeping cellular functions and growth. Respiration is composed of three pathways, the glycolysis degrading sugars, the TCA cycle metabolises sugar by-products to produce redox energy that will be used by the oxidative phosphorylation (OXPHOS) system to convert ADP into ATP. The reactions leading to ATP synthesis are well understood but the mechanisms involved in the regulation of this pathway remain unclear. In addition to the ATP production, the respiratory activity influences other metabolic pathways. However, it is unknown if the respiratory activity can actively or passively modulate the cellular metabolism. Two hypotheses have been formulated to explain how respiratory activity affects cellular metabolic reactions. As the main ATP producing pathway, respiration has a direct impact on the ATP/ADP ratio and on the activity of enzymes using ATP. This control of enzyme activity by the ATP/ADP ratio is known as the adenylate control. Besides, the OXPHOS system is producing reactive oxygen species (ROS) when electrons are lost. As ROS accumulation causes a modification of the redox status, the modulation of cellular metabolism by the activity of the OXPHOS system via ROS/redox signaling is another possibility. This project aimed to understand how the respiratory chain contributes to the control of plant metabolism. To achieve this goal, we used mutants in the first complex of the OXPHOS system, complex I, in the model plant Arabidopsis thaliana. Complex I is not described as essential for plant growth but complex I mutants show a growth retardation. We built a collection of complex I mutants and identified strong and mild mutants based on the severity of the growth phenotype. We characterized these mutants using a systems biology approach, which explores steady-state levels, to identify the mitochondrial signal(s) triggering a cellular response, hypothesizing that the strong mutants should express stronger signals. However this approach did not yield the expected outcome as the mutants studied, despite showing severe phenotypic differences, were found to be extremely similar at a molecular level. However, an intensive characterization of the mutants allowed the identification of differences in fluxes through the respiratory pathway between strong and mild complex I mutants. In addition, our work shows that complex I is essential for a key development step. In conclusion, during the course of this project we showed that complex I is essential for survival in plants as it is in mammals. In addition, we showed that in the absence of complex I, respiration fluxes are impaired, suggesting that complex I acts as a negative regulator of respiration. This finding, if it is confirmed in humans, could be the basis of the development of new treatment strategies to cure the multiple diseases caused by complex I deficiency.