Respiration plays a key role in the survival of aerobic organisms since it is providing ATP, the energy for the whole cell. The reactions leading to the synthesis of ATP are well known but the mechanisms by which mitochondrial respiration controls cellular functions is unknown, mainly because most mutants in respiratory enzymes are lethal. Two hypotheses have been formulated to explain how respiration activity affects the metabolism. As the product of respiration is ATP, the respiration rate has an 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 mitochondrial electron transfer chain (ETC) is producing reactive oxygen species (ROS) when electrons are lost during their transfer through the ETC. As ROS accumulation causes a modification of the redox status and triggers the reorganisation of cellular activity, therefore the influence of ETC activity on cellular metabolism via ROS signalling is another possibility. In plants, most of the mutants with impaired respiration are affected in complex I, the first enzyme of the ETC. These mutants have reduced ATP synthesis and enhanced stress tolerance, indicating that both the adenylate control and the ROS signalling are affected. This project aims to understand how respiration contributes to the control of plant metabolism. Several complex I mutants which possess different levels of remaining complex I activity are available in Arabidopsis. The production of ATP and ROS by the ETC will be investigated to characterise the respiratory defect caused by the reduction in complex I function. System biology approaches including transcriptomic and metabolomic will be use to highlight the mitochondrial signals causing a cellular response and elucidate the corresponding pathways with a special attention to the adenylate control and the ROS signalling pathway.