Roles, Regulation, and Agricultural Application of Plant Phosphate Transporters

Abstract

Phosphorus (P) is an essential mineral nutrient for plant growth and development. Low availability of inorganic phosphate (orthophosphate; Pi) in soil seriously restricts the crop production, while excessive fertilization has caused environmental pollution. Pi acquisition and homeostasis depend on transport processes controlled Pi transporters, which are grouped into five families so far: PHT1, PHT2, PHT3, PHT4, and PHT5. This review summarizes the current understanding on plant PHT families, including phylogenetic analysis, function, and regulation. The potential application of Pi transporters and the related regulatory factors for developing genetically modified crops with high phosphorus use efficiency (PUE) are also discussed in this review. At last, we provide some potential strategies for developing high PUE crops under salt or drought stress conditions, which can be valuable for improving crop yields challenged by global scarcity of water resources and increasing soil salinization.

Keywords: Eutrema salsugineum; crop; drought; genetic modification; low phosphate; phosphate transporter; regulation; salinity.

FIGURE 1

Phylogenetic analysis of Pi transporters. The phylogenetic tree was constructed by the Neighbor-Joining method with MEGA6.0, bootstrap values are from 1000 replicates. Accession numbers or locus IDs of all used proteins were given in Supplementary Table S1.

FIGURE 2

Simplified models for the post-transcriptional and post-translational regulation of PHT1 transporters. Under Pi-replete condition, phosphorylation of PHT1 transporters prevents their exit from ER and the subsequent targeting to the PM. NLA and PHO2 direct the ubiquitin-mediated degradation of PHT1 transporters at PM and ER, respectively, to avoid excessive accumulation of Pi. Under Pi deficiency condition, miR827 and miR399 mediate cleavage of NLA and PHO2 transcripts, respectively, thus to increase the amount of PHT1 transporters. PHF1 is accounted for the PHT1 transporters exit from ER and correct targeting to PM.