A genetic analysis of phosphate deficiency responses in Arabidopsis.

摘要

Inorganic phosphate (Pi) plays a central role in metabolism. It is a structural constituent of biomolecules such as nucleic acids and phospholipids and functions as reactant and allosteric regulator in carbon metabolism and signal transduction. Consequently, Pi availability has a direct and profound impact on plant performance and crop productivity. To cope with Pi shortage, which is a frequent problem on account of its low solubility in soils, plants activate a set of adaptive responses that optimize Pi economy by reprogramming metabolism for conservation and remobilization. In order to enhance soil exploration and increase Pi uptake, plants respond by remodeling root system architecture. Although physiological responses to Pi limitation have been the subject of extensive study, our understanding of the molecular mechanisms that plants use to monitor Pi status and integrate plant responses is fragmentary at best.; We have taken a genetic approach to dissecting Pi sensing using the plant model organism Arabidopsis thaliana. We have identified a class of phosphate deficiency response (pdr) mutants that is characterized by a hypersensitive response to Pi limitation. Detailed analysis of the pdr2 primary root reveals an inhibition of cell division in response to Pi limitation that is followed by meristem consumption and cell death. All higher order root meristems of pdr2 initiate normally and form fully functional meristems, which then arrest at the developmental stage of meristem maintenance, suggesting a switch in root development when roots begin to monitor external Pi. The consumption of the pdr2 root apical meristem during Pi starvation is at least partially due to the differentiation of meristematic stem cells.; PDR2 encodes At5g23630, the single P-type ATPase of group 5 in Arabidopsis, AtP5. The function of P5-type ATPases in plants is unknown. Although none of the plant P-type ATPases studied to date is known to transport anions, the phenotype of the pdr2 mutant, which is highly specific to conditions of phosphate starvation, suggests that the AtP5 ATPase may play a role in the regulation of Pi homeostasis.