Respiration

The rate of plant respiration is linked to the rate of metabolism and growth due to requirements for ATP, reductant, and carbon skeletons during cell maintenance, division, and expansion.). Light is known to regulate gene expression of several key respiratory enzymes through the action of phytochrome, including cytochrome c oxidase and phosphoenolpyruvate carboxylase. It has also been suggested that blue light can cause an increase in total respiration. Furthermore, there is a differential expression of alternative oxidase genes between light grown and dark grown tissues. While there is broad agreement that higher atmospheric CO₂ levels stimulate photosynthesis in C3 plants, such as soybean, no such consensus exists on how rising CO₂ levels will affect plant respiration. Respiration rates were generally sensitive to short term changes in the measurement carbon dioxide concentration for plants grown at the lowest, but not the highest carbon dioxide concentration. At all temperatures, growth at elevated carbon dioxide concentrations decreased total respiration measured at the growth concentration, with no significant differences among cultivars.). Although net photosynthesis decreased by 40% and 70% under mild and severe water stress, respectively, the total respiratory oxygen uptake (V _t) was not significantly different at any water-stress level. However, severe water stress caused a significant shift of electrons from the cytochrome to the alternative pathway. The respiration rate of the central tissue of the nodule is almost entirely determined by the rate of oxygen diffusion to the respiratory enzymes.Evidence is given that the nodule cortex is the site of almost all the resistance to oxygen diffusion within the nodule. Waterlogging blocks the oxygen supply to the root system which inhibits respiration, and greatly reduces the energy status of cells that affect important metabolic processes. Nodule mitochondria are highly sensitive to the respiratory inhibitor antimycin A. The antimycin-resistant oxygen uptake is 5–10% of the rate of control mitochondrial respiration. The high sensitivity to this inhibitor means that non-phosphorylating pathways are absent from the nodules and the energetic effectiveness of mitochondria is very high.