Orthophosphate (Pi) is an essential macronutrient that plays a central role in virtually all major metabolic processes in plants, particularly photosynthesis and respiration. Many metabolites are Pi monoesters, whereas the phosphoanhydride bonds of compounds such as ATP function to transfer energy from the energyyielding process of photo-, oxidative, and substratelevel phosphorylation to the energy-dependent cellular processes of biosynthesis, ion pumping, and mechanical work. The massive use of Pi-containing fertilizers in agriculture demonstrates how the soluble Pi level of many soils is suboptimal for crop growth. Accessible reserves of rock phosphate-our major source of Pi fertilizers-are projected to be exhausted by the end of this century (Vance et al., 2003). The use of Pi fertilizers is also quite inefficient with less than 20% of applied Pi being absorbed by plants during their first growing season. The remaining Pi becomes immobile in the soil or leaches into and pollutes nearby surface waters. Agricultural Pi runoff is a primary factor in the eutrophication of lakes and marine estuaries, and has also resulted in blooms of toxic cyanobacteria. With the world's population continuing its rapid increase, mankind faces a daunting challenge to produce sufficient food crops in the face of dwindling supplies of Pi fertilizers. A more comprehensive understanding of the biochemical and physiological mechanisms of plant Pi uptake and use is leading to the development of rational strategies and molecular tools for engineering nutrient-efficient cultivars needed to reduce agriculture's overreliance on unsustainable Pi fertilizers. The aim of this Update article is to consider the influence of Pi nutrition on plant metabolism, with a focus on adaptive metabolic responses that serve to ameliorate the negative side effects of Pi deficiency. Examples of how metabolic Pi scavenging and recycling, and the unique flexibility of plant metabolism and bioenergetics may contribute to the survival of Pideficient (2Pi) plants are highlighted.

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Plant purple acid phosphatases (PAPs) belong to a large multigene family whose specific functions in Pi metabolism are poorly understood. Two PAP isozymes secreted by Pi-deficient (-Pi) Arabidopsis thaliana were purified from culture filtrates of -Pi suspension cells. They correspond to an AtPAP12 (At2g27190) homodimer and AtPAP26 (At5g34850) monomer composed of glycosylated 60 and 55 kDa subunit(s), respectively. Each PAP exhibited broad pH activity profiles centred at pH 5.6, and overlapping substrate specificities. Concanavalin-A chromatography resolved a pair of secreted AtPAP26 glycoforms. AtPAP26 is dual targeted during Pi stress because it is also the principal intracellular (vacuolar) PAP up-regulated by -Pi Arabidopsis. Differential glycosylation appears to influence the subcellular targeting and substrate selectivity of AtPAP26. The significant increase in secreted acid phosphatase activity of -Pi seedlings was correlated with the appearance of immunoreactive AtPAP12 and AtPAP26 polypeptides. Analysis of atpap12 and atpap26 T-DNA mutants verified that AtPAP12 and AtPAP26 account for most of the secreted acid phosphatase activity of -Pi wild-type seedlings. Semi-quantitative RT-PCR confirmed that transcriptional controls exert little influence on the up-regulation of AtPAP26 during Pi stress, whereas AtPAP12 transcripts correlate well with relative levels of secreted AtPAP12 polypeptides. We hypothesize that AtPAP12 and AtPAP26 facilitate Pi scavenging from soil-localized organophosphates during nutritional Pi deprivation.

MPAN is caused by mutations in C19orf12 leading to NBIA and prominent, widespread Lewy body pathology. The clinical phenotype is recognizable and distinctive, and joins pantothenate kinase-associated neurodegeneration and PLA2G6-associated neurodegeneration as one of the major forms of NBIA.