Contents Summary306I.The need to use phosphorus efficiently307II.P‐use efficiency and P dynamics in a growing crop307III.P pools in plants307IV.Phosphorus pools and growth rates310V.Are crops different from other plants in their P concentration?310VI.Phosphorus use and photosynthesis311VII.Crop development and canopy P distribution312VIII.Internal redistribution of P in a growing vegetative plant313IX.Allocation of P to reproductive structures314X.Constraints to P remobilisation315XI.Do physiological or phylogenetic trade‐offs constrain traits that could improve PUE?316XII.Identifying genetic loci associated with PUE316XIII.Conclusions317Acknowledgements317References317 Summary Limitation of grain crop productivity by phosphorus (P) is widespread and will probably increase in the future. Enhanced P efficiency can be achieved by improved uptake of phosphate from soil (P‐acquisition efficiency) and by improved productivity per unit P taken up (P‐use efficiency). This review focuses on improved P‐use efficiency, which can be achieved by plants that have overall lower P concentrations, and by optimal distribution and redistribution of P in the plant allowing maximum growth and biomass allocation to harvestable plant parts. Significant decreases in plant P pools may be possible, for example, through reductions of superfluous ribosomal RNA and replacement of phospholipids by sulfolipids and galactolipids. Improvements in P distribution within the plant may be possible by increased remobilization from tissues that no longer need it (e.g. senescing leaves) and reduced partitioning of P to developing grains. Such changes would prolong and enhance the productive use of P in photosynthesis and have nutritional and environmental benefits. Research considering physiological, metabolic, molecular biological, genetic and phylogenetic aspects of P‐use efficiency is urgently needed to allow significant progress to be made in our understanding of this complex trait.

The two forms of inorganic arsenic, arsenate (AsV) and arsenite (AsIII), are easily taken up by the cells of the plant root. Once in the cell, AsV can be readily converted to AsIII, the more toxic of the two forms. AsV and AsIII both disrupt plant metabolism, but through distinct mechanisms. AsV is a chemical analog of phosphate that can disrupt at least some phosphate-dependent aspects of metabolism. AsV can be translocated across cellular membranes by phosphate transport proteins, leading to imbalances in phosphate supply. It can compete with phosphate during phosphorylation reactions, leading to the formation of AsV adducts that are often unstable and short-lived. As an example, the formation and rapid autohydrolysis of AsV-ADP sets in place a futile cycle that uncouples photophosphorylation and oxidative phosphorylation, decreasing the ability of cells to produce ATP and carry out normal metabolism. AsIII is a dithiol reactive compound that binds to and potentially inactivates enzymes containing closely spaced cysteine residues or dithiol co-factors. Arsenic exposure generally induces the production of reactive oxygen species that can lead to the production of antioxidant metabolites and numerous enzymes involved in antioxidant defense. Oxidative carbon metabolism, amino acid and protein relationships, and nitrogen and sulfur assimilation pathways are also impacted by As exposure. Readjustment of several metabolic pathways, such as glutathione production, has been shown to lead to increased arsenic tolerance in plants. Species- and cultivar-dependent variation in arsenic sensitivity and the remodeling of metabolite pools that occurs in response to As exposure gives hope that additional metabolic pathways associated with As tolerance will be identified.

Juvenile Paget's disease can result from osteoprotegerin deficiency caused by homozygous deletion of TNFRSF11B.

The effect of water stress on respiration and mitochondrial electron transport has been studied in soybean (Glycine max) leaves, using the oxygen-isotope-fractionation technique. Treatments with three levels of water stress were applied by irrigation to replace 100%, 50%, and 0% of daily water use by transpiration. The levels of water stress were characterized in terms of lightsaturated stomatal conductance (g s ): well irrigated (g s . . 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 electron partitioning through the alternative pathway increased from 10% to 12% under well-watered or mild water-stress conditions to near 40% under severe water stress. Consequently, the calculated rate of mitochondrial ATP synthesis decreased by 32% under severe water stress. Unlike many other stresses, water stress did not affect the levels of mitochondrial alternative oxidase protein. This suggests a biochemical regulation (other than protein synthesis) that causes this mitochondrial electron shift.Water stress is considered one of the most important factors limiting plant performance and yield worldwide (Boyer, 1982). Effects of water stress on a plant's physiology, including growth (McDonald and Davies, 1996), signaling pathways (Chaves et al., 2003), gene expression (Bray, 1997(Bray, , 2002, and leaf photosynthesis (Lawlor and Cornic, 2002;Flexas et al., 2004), have been studied extensively. Surprisingly, compared with other physiological processes, studies examining the effects of water stress on respiration are few (Hsiao, 1973; Amthor, 1989), despite the importance of respiration in ecosystem annual net productivity (Valentini et al., 1999) and the fact that ecosystem respiration is strongly affected by water availability (Bowling et al., 2002). Another important point to consider is the effect of water stress on the electron partitioning between the cytochrome and the cyanide-resistant, alternative pathway and its consequences for ATP synthesis. Unfortunately, the few studies that have focused on alternative respiration as affected by water stress (Zagdańska, 1995;Collier and Cummins, 1996; González-Meler et al., 1997) used specific inhibitors for the cytochrome (KCN) and alternative (salicylhydroxamic acid [SHAM]) respiratory pathways; this methodology is now known to be invalid (Millar et al., 1995;Day et al., 1996;Lambers et al., 2005). Currently, the only available system to measure electron partitioning between the two respiratory pathways and their actual activities is the use of the oxygen-isotope-fractionation technique McDonald et al., 2003;Ribas-Carbo et al., 2005). This technique is based on the fact that the two terminal oxidases fractionate 18 O differently, with the cytochrome oxidase discriminating less than the alternative oxid...