Significance: Phosphate is an essential nutrient for plant growth, and inorganic phosphate (Pi) is stored largely in the vacuole of plant cells. Thus, vacuolar Pi maintains homeostasis of cytosolic Pi to ensure an optimal Pi supply for plants under variable Pi status in the soil. This study uncovered inArabidopsisa vacuolar phosphate transporter, VPT1, that mediates vacuolar Pi sequestration. Lack of VPT1 caused growth defects under both low-Pi and high-Pi conditions, implicating VPT1 in plant adaptation to constantly changing Pi levels in the environment. This finding not only supplies a missing link in our understanding of vacuolar Pi storage and homeostasis, but also provides a new path for engineering crops that can better adapt to variable Pi availability in the soil.

Polyamines are known to increase in plant cells in response to a variety of stress conditions. However, the physiological roles of elevated polyamines are not understood well. Here we investigated the effects of polyamines on ion channel activities by applying patch-clamp techniques to protoplasts derived from barley (Hordeum vulgare) seedling root cells. Extracellular application of polyamines significantly blocked the inward Na⁺ and K⁺ currents (especially Na⁺ currents) in root epidermal and cortical cells. These blocking effects of polyamines were increased with increasing polycation charge. In root xylem parenchyma, the inward K⁺ currents were blocked by extracellular spermidine, while the outward K⁺ currents were enhanced. At the whole-plant level, the root K⁺ content, as well as the root and shoot Na⁺ levels, was decreased significantly by exogenous spermidine. Together, by restricting Na⁺ influx into roots and by preventing K⁺ loss from shoots, polyamines were shown to improve K⁺/Na⁺ homeostasis in barley seedlings. It is reasonable to propose that, therefore, elevated polyamines under salt stress should be a self-protecting response for plants to combat detrimental consequences resulted from imbalance of Na⁺ and K⁺.

Cadmium (Cd²⁺) interferes with the uptake, transport and utilization of several macro‐ and micronutrients, which accounts, at least in part, for Cd²⁺ toxicity in plants. However, the mechanisms underlying Cd²⁺ interference of ionic homeostasis is not understood. Using biophysical techniques including membrane potential measurements, scanning ion‐selective electrode technique for non‐invasive ion flux assays and patch clamp, we monitored the effect of Cd²⁺ on calcium (Ca²⁺) and potassium (K⁺) transport in root hair cells of rice. Our results showed that K⁺ and Ca²⁺ contents in both roots and shoots were significantly reduced when treated with exogenous Cd²⁺. Further studies revealed that three cellular processes may be affected by Cd²⁺, leading to changes in ionic homeostasis. First, Cd²⁺‐induced depolarization of the membrane potential was observed in root hair cells, attenuating the driving force for cation uptake. Second, the inward conductance of Ca²⁺ and K⁺ was partially blocked by Cd²⁺, decreasing uptake of K⁺ and Ca²⁺. Third, the outward K⁺ conductance was Cd²⁺‐inducible, decreasing the net content of K⁺ in roots. These results provide direct evidence that Cd²⁺ impairs uptake of Ca²⁺ and K⁺, thereby disturbing ion homeostasis in plants.

Significance: Turgor pressure is the driving force for cell growth in plants, and the large central vacuole provides the major space for turgor regulation. However, the molecular identity and function of many transporters that control water and solute fluxes in and out of vacuoles remain unknown. We report here that two Multidrug and Toxic Compound Extrusion (MATE)-type transporters show previously unrecognized function as chloride channels essential for turgor regulation in Arabidopsis . The MATE transporters are highly conserved from bacteria, fungi, plants, to animals, and widely accepted as transporters of organic compounds. This study, showing some MATE transporters as chloride channels, thus breaks the old dogma on the functional definition of this large family of transporters.

The plant elicitor peptides (Peps), a family of damage/danger-associated molecular patterns (DAMPs), are perceived by two receptors, PEPR1 and PEPR2, and contribute to plant defense against pathogen attack and abiotic stress. Here we show that the Peps-PEPR signaling pathway functions in stomatal immunity by activating guard cell anion channels in Arabidopsis thaliana. The mutant plants lacking both PEPR1 and PEPR2 (pepr1 pepr2) displayed enhanced bacterial growth after being sprayed with Pseudomonas syringae pv. tomato (Pst) DC3000, but not after pathogen infiltration into leaves, implicating PEPR function in stomatal immunity. Indeed, synthetic Arabidopsis Peps (AtPeps) effectively induced stomatal closure in wild-type but not pepr1 pepr2 mutant leaves, suggesting that the AtPeps-PEPR signaling pathway triggers stomatal closure. Consistent with this finding, patch-clamp recording revealed AtPep1-induced activation of anion channels in the guard cells of wild-type but not pepr1 pepr2 mutant plants. We further identified two guard cell-expressed anion channels SLOW ANION CHANNEL 1 (SLAC1) and its homologue SLAH3, as functionally overlapping components responsible for AtPep1-induced stomatal closure. The slac1 slah3 double mutant, but not slac1 or slah3 single mutants, failed to respond to AtPep1 in stomatal closure assays. Interestingly, disruption of OPEN STOMATA 1 (OST1), an essential gene for abscisic acid-triggered stomatal closure, did not affect the AtPep1-induced anion channel activity and stomatal response. Together, these results illustrate a DAMP-triggered signaling pathway that, unlike the flagellin22-FLAGELLIN-SENSITIVE 2 pathway, triggers stomata immunity through an OST1-independent mechanism.

In Arabidopsis, the salt overly sensitive (SOS) pathway, consisting of calcineurin B-like protein 4 (CBL4/SOS3), CBL-interacting protein kinase 24 (CIPK24/SOS2) and SOS1, has been well defined as a crucial mechanism to control cellular ion homoeostasis by extruding Na⁺ to the extracellular space, thus conferring salt tolerance in plants. CBL10 also plays a critical role in salt tolerance possibly by the activation of Na⁺ compartmentation into the vacuole. However, the functional relationship of the SOS and CBL10-regulated processes remains unclear. Here, we analyzed the genetic interaction between CBL4 and CBL10 and found that the cbl4 cbl10 double mutant was dramatically more sensitive to salt as compared to the cbl4 and cbl10 single mutants, suggesting that CBL4 and CBL10 each directs a different salt-tolerance pathway. Furthermore, the cbl4 cbl10 and cipk24 cbl10 double mutants were more sensitive than the cipk24 single mutant, suggesting that CBL10 directs a process involving CIPK24 and other partners different from the SOS pathway. Although the cbl4 cbl10, cipk24 cbl10, and sos1 cbl10 double mutants showed comparable salt-sensitive phenotype to sos1 at the whole plant level, they all accumulated much lower Na⁺ as compared to sos1 under high salt conditions, suggesting that CBL10 regulates additional unknown transport processes that play distinct roles from the SOS1 in Na⁺ homeostasis.