Phosphate Uptake and Transport in Plants

Phosphorus (P) is an indispensable macronutrient for plant growth, development, and reproduction. It is a component of crucial biomolecules such as DNA, RNA, ATP, NADPH, and phospholipids.

Form for Uptake: Plants primarily absorb P from the soil as inorganic phosphate (Pi, specifically H₂PO₄^- or HPO₄^2-).

Availability Challenge: Pi is often sequestered (fixed) in the soil by Fe3+ and Al3+ (acidic soils) or by tricalcium (alkaline soils), resulting in low availability and mobility for the plant.

P Starvation Responses (PSRs)

Plants have evolved sophisticated adaptive mechanisms, called phosphate starvation responses (PSRs), to enhance the acquisition of external P and improve the utilization of internal P.

A. Enhanced Acquisition of External P (Local PSRs)

These responses are regulated by the external P concentration around the root.

1. Root System Architecture (RSA) Modification:

   • Increased number of lateral roots and root hairs.

   • Reduction of primary root growth.

   • Formation of proteoid roots (dense cluster of rootlets).

   • Goal: Efficiently forage for P in the topsoil and enlarge the root-soil surface area.

2. Increased Pi Release and Uptake:

   • Roots secrete organic acids, nucleases, and phosphatases to release Pi from insoluble or organic matter.

   • Increased activity of high-affinity Pi transporters (PHT1) in the root surface to facilitate Pi uptake.

3. Beneficial Interactions: Facilitating interactions with beneficial microbes, such as arbuscular mycorrhizal fungi, promotes P acquisition.

Proteoid root formation under Pi deficiency

B. Improved Utilization of Internal P (Systemic PSRs)

These responses depend on adjusting the internal P concentration to optimize P recycling and reallocation.

1. Growth Adjustment: Increase the root-to-shoot growth ratio to adapt to P deficiency.

2. Pi Reallocation: Increase the xylem loading activity of Pi to facilitate root-to-shoot reallocation. PHO1 is a key protein in this process.

3. Metabolic Adaptations:

   • Replacement of phospholipids with galacto- and sulfolipids.

   • Activation of metabolic bypasses to conserve ATP.

4. Storage Modulation: Regulating vacuolar Pi storage and release to maintain cytosolic Pi homeostasis.

Phosphate Transporters

Pi transporters are essential proteins that facilitate Pi transport across membranes for uptake, distribution, and remobilization.

A. PHT (Phosphate Transporter) Family

This is the largest family, classified into five types based on subcellular localization:

Transporter Family	Subcellular Location(s)	Function	Mechanism
PHT1	Plasma membrane	Pi acquisition from soil; Pi translocation between tissues	H+-Pi symporters, High-affinity Pi transporters
PHT2	Chloroplasts	Pi homeostasis within the organelle	Low affinity Pi transporter, H+-Pi symporters or Na+-Pi symporters
PHT3	Mitochondria	Pi homeostasis within the organelle	Pi exchange between mitochondria and cytosol by Pi/H+ symport or Pi/OH- antiport
PHT4	Golgi apparatus, Chloroplasts, Non-photosynthetic plastids	Pi homeostasis within the organelles	Low affinity Pi transporter, H+-Pi symporters or Na+-Pi symporters
PHT5/VPT1	Vacuole (Tonoplast)	Pi influx and storage	SPX-MFS domain protein

 

B. Other Transporters

Transporter Name	Family Type	Location	Function
PHO1	SPX-EXS domain protein	Plasma membrane, Golgi	Pi efflux transporter mediating root-to-shoot Pi translocation (loading into the xylem)
VPE (VACUOLAR PHOSPHATE EFFLUX)	SPX-MFS domain protein	Vacuole (Tonoplast)	Pi efflux (release from storage)
SPDT (SULTR-like P Distribution Transporter)	SULTR-like family	Plasma membrane	Involved in Pi uptake and translocation

Regulation of Pi Uptake and Transport

Pi transporters are tightly controlled at the transcriptional and posttranslational levels.

A. Transcriptional Regulation

• PHR proteins: PHOSPHATE STARVATION RESPONSE (PHR) proteins are central transcriptional regulators. They bind to the P1BS (PHR1 binding sequence, GNATATNC) element to upregulate the transcription of PHT1and other PSR genes under P starvation.

B. Post-Translational Regulation (Trafficking and Degradation)

1. Protein Trafficking to the Membrane:

   • PHF1 (PHOSPHATE TRANSPORTER TRAFFIC FACILITATOR 1): Required for the proper exit of PHT1 proteins from the endoplasmic reticulum (ER) to the plasma membrane.

2. Protein Degradation (Turnover):

   • PHO2 (PHOSPHATE 2): A ubiquitin E2 conjugase that controls the protein abundance of PHT1 and PHO1 by mediating their degradation, a process regulated by cellular P status.

   • NLA (NITROGEN LIMITATION ADAPTATION): A RING-type E3 ligase with an SPX domain that mediates PHT1 degradation at the plasma membrane.

C. Systemic Signaling: The miR399-PHO2 Axis

• P Starvation Signal: Under P starvation, the non-coding RNA microRNA399 (miR399) is upregulated.

• Shoot-to-Root Movement: miR399 acts as a shoot-to-root systemic signal.

• Mechanism: In the root, miR399 suppresses the expression of the PHO2 gene.

• Outcome: The reduction in PHO2 protein leads to the stabilization (reduced degradation) of its targets, including PHT1 and PHO1. This results in enhanced Pi uptake and translocation.