Mitochondria play a central role in aerobic respiration and energy metabolism in complex organisms. The mitochondrial energy metabolism, in turn, is the major source of reactive oxygen species (ROS). In order to deal with the high generation of ROS and its consequences to the cellular metabolism, mitochondria holds a powerful antioxidant machinery that acts inside the organelle, but reflects in several cellular compartments. Among the components of this machinery, there is the mitochondrial uncoupling proteins (UCPs) that are located at the mitochondrial inner membrane and allow the free flow of protons from the intermembrane space toward the mitochondrial matrix. When the proton gradient is dissipated, the electron flux across the electron transport chain (ETC) is stimulated and ROS generation decreases. The overexpression of UCP1 in plants is associated with a global cellular response that involves the mechanism of mitochondrial biogenesis together with the up-regulation of genes related to stress responses and alteration in the photosynthetic metabolism. Recent studies show that plants overexpressing UCP1 assimilate more CO2 than wild type plants. Nevertheless, transcriptomic profiling of these plants revealed the down-regulation of genes involved in photosynthesis. Among these genes, there are the ones responsible for coding components of the photosystems (PS) I and II, a contrasting fact, since PS-I and II are essential for the production of NADPH that is used in the Calvin cycle. The aim of this project is to investigate the changes caused by the overexpression of UCP1 in the photosynthetic metabolism at a protein and metabolic level. It will be taken into account parameters such as the photosynthetic efficiency, PSI and PSII protein levels, the NADPH/NADP ratio and the amount of carbohydrates and chlorophyll in different transgenic lines of Nicotiana tabacum overexpressing UCP1 in comparison with wild type plants.
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