The capacity of plants to maintain a high cytosolic K + /Na + ratio is likely to be one of the key determinants of plant salt tolerance. Important p

Although not essential for most plants, sodium (Na⁺) can be beneficial to plants in many conditions, particularly when potassium (K⁺) is deficient. As such it can be regarded a ‘non-essential’ or ‘functional’ nutrient. By contrast, the many salinized areas around the globe force plants to deal with toxicity from high levels of Na⁺ in the environment and within tissues. Progress has been made in identifying the relevant membrane transporters involved in the uptake and distribution of Na⁺. The latter is important in the context of mitigating salinity stress but also for the optimization of Na⁺ as an abundantly available functional nutrient. In both cases plants are likely to require mechanism(s) to monitor Na⁺ concentration, possibly in multiple compartments, to regulate gene expression and transport activities. Extremely little is known about whether such mechanisms are present and if so, how they operate, either at the cellular or the tissue level. This paper gives an overview of the regulatory and potential sensing mechanisms that pertain to Na⁺, in both the context of salt stress and Na⁺ as a nutrient.

The Arabidopsis thaliana genome contains five genes that encode two pore K ⁺ (TPK) channels. The most abundantly expressed isoform of this family, TPK1, is expressed at the tonoplast where it mediates K ⁺ -selective currents between cytoplasmic and vacuolar compartments. TPK1 open probability depends on both cytoplasmic Ca ²⁺ and cytoplasmic pH but not on the tonoplast membrane voltage. The channel shows intrinsic rectification and can be blocked by Ba ²⁺ , tetraethylammonium, and quinine. TPK1 current was found in all shoot cell types and shows all of the hallmarks of the previously described vacuolar K (VK) tonoplast channel characterized in guard cells. Characterization of TPK1 loss-of-function mutants and TPK1-overexpressing plants shows that TPK1 has a role in intracellular K ⁺ homeostasis affecting seedling growth at high and low ambient K ⁺ levels. In stomata, TPK1 function is consistent with vacuolar K ⁺ release, and removal of this channel leads to slower stomatal closure kinetics. During germination, TPK1 contributes to the radicle development through vacuolar K ⁺ deposition to provide expansion growth or in the redistribution of essential minerals.

The Arabidopsis thaliana genome contains 20 cyclic nucleotide gated channel (CNGC) genes encoding putative non-selective ion channels. Classical and reverse genetic approaches have revealed that two members of this family (CNGC2 and CNGC4) play a role in plant defence responses whereas CNGC1 and CNGC10 may participate in heavy metal and cation transport. Yet, it remains to be resolved how the ion transport attributes of CNGCs are integrated into their physiological function. In this study, CNGC3 is characterized through heterologous expression, GUS- and GFP-reporter gene fusions, and by adopting a reverse genetics approach. A CNGC3–GFP fusion protein shows that it is mainly targeted to the plasma membrane. Promoter GUS studies demonstrate CNGC3 expression predominantly in the cortical and epidermal root cells, but also a ubiquitous presence in shoot tissues. Expression of CNGC3 in yeast indicates it can function as a Na⁺ uptake and a K⁺ uptake mechanism. cngc3 null mutations decreased seed germination in the presence of NaCl but not KCl. Relative to the wild type, mutant seedling growth is more resistant to the presence of toxic concentrations of NaCl and KCl. The ionic composition and ion uptake characteristics of wild-type and mutant seedlings suggests that the growth advantage in these conditions may be due to restricted ion influx in mutant plants, and that CNGC3 functions in the non-selective uptake of monovalent cations in Arabidopsis root tissue.

When exposed to salt, every plant takes up Na+ from the environment. Once in the symplast, Na+ is distributed within cells and between different tissues and organs. There it can help to lower the cellular water potential but also exert potentially toxic effects. Control of Na+ fluxes is therefore crucial and indeed, research shows that the divergence between salt tolerant and salt sensitive plants is not due to a variation in transporter types but rather originates in the control of uptake and internal Na+ fluxes. A number of regulatory mechanisms has been identified based on signalling of Ca2+, cyclic nucleotides, reactive oxygen species, hormones, or on transcriptional and post translational changes of gene and protein expression. This review will give an overview of intra- and intercellular movement of Na+ in plants and will summarise our current ideas of how these fluxes are controlled and regulated in the early stages of salt stress.