Summary: Agriculture is expanding into regions that are affected by salinity. This review considers the energetic costs of salinity tolerance in crop plants and provides a framework for a quantitative assessment of costs. Different sources of energy, and modifications of root system architecture that would maximize water vs ion uptake are addressed. Energy requirements for transport of salt (NaCl) to leaf vacuoles for osmotic adjustment could be small if there are no substantial leaks back across plasma membrane and tonoplast in root and leaf. The coupling ratio of the H⁺‐ATPase also is a critical component. One proposed leak, that of Na⁺ influx across the plasma membrane through certain aquaporin channels, might be coupled to water flow, thus conserving energy. For the tonoplast, control of two types of cation channels is required for energy efficiency. Transporters controlling the Na⁺ and Cl⁻ concentrations in mitochondria and chloroplasts are largely unknown and could be a major energy cost. The complexity of the system will require a sophisticated modelling approach to identify critical transporters, apoplastic barriers and root structures. This modelling approach will inform experimentation and allow a quantitative assessment of the energy costs of NaCl tolerance to guide breeding and engineering of molecular components.

The root growth of most crop plants is inhibited by soil salinity. Roots respond by modulating metabolism, gene expression and protein activity, which results in changes in cell wall composition, transport processes, cell size and shape, and root architecture. Here, we focus on the effects of salt stress on cell wall modifying enzymes, cellulose microfibril orientation and non-cellulosic polysaccharide deposition in root elongation zones, as important determinants of inhibition of root elongation, and highlight cell wall changes linked to tolerance to salt stressed and water limited roots. Salt stress induces changes in the wall composition of specific root cell types, including the increased deposition of lignin and suberin in endodermal and exodermal cells. These changes can benefit the plant by preventing water loss and altering ion transport pathways. We suggest that binding of Na+ ions to cell wall components might influence the passage of Na+ and that Na+ can influence the binding of other ions and hinder the function of pectin during cell growth. Naturally occurring differences in cell wall structure may provide new resources for breeding crops that are more salt tolerant.

Silicon application can improve productivity outcomes for salt stressed plants. Here, we describe how strawberry plants respond to treatments including various combinations of salt stress and nano-silicon dioxide, and assess whether nano-silicon dioxide improves strawberry plant tolerance to salt stress. Strawberry plants were treated with salt (0, 25 or 50 mM NaCl), and the nano-silicon dioxide treatments were applied to the strawberry plants before (0, 50 and 100 mg L⁻¹) or after (0 and 50 mg L⁻¹) flowering. The salt stress treatments reduced plant biomass, chlorophyll content, and leaf relative water content (RWC) as expected. Relative to control (no NaCl) plants the salt treated plants had 10% lower membrane stability index (MSI), 81% greater proline content, and 54% greater cuticular transpiration; as well as increased canopy temperature and changes in the structure of the epicuticular wax layer. The plants treated with nano-silicon dioxide were better able to maintain epicuticular wax structure, chlorophyll content, and carotenoid content and accumulated less proline relative to plants treated only with salt and no nano-silicon dioxide. Analysis of scanning electron microscopic (SEM) images revealed that the salt treatments resulted in changes in epicuticular wax type and thickness, and that the application of nano-silicon dioxide suppressed the adverse effects of salinity on the epicuticular wax layer. Nano-silicon dioxide treated salt stressed plants had increased irregular (smoother) crystal wax deposits in their epicuticular layer. Together these observations indicate that application of nano-silicon dioxide can limit the adverse anatomical and biochemical changes related to salt stress impacts on strawberry plants and that this is, in part, associated with epicuticular wax deposition.

Summary: Bread wheat (Triticum aestivum L.) has a major salt tolerance locus, Kna1, responsible for the maintenance of a high cytosolic K⁺/Na⁺ ratio in the leaves of salt stressed plants. The Kna1 locus encompasses a large DNA fragment, the distal 14% of chromosome 4DL. Limited recombination has been observed at this locus making it difficult to map genetically and identify the causal gene. Here, we decipher the function of TaHKT1;5‐D, a candidate gene underlying the Kna1 locus. Transport studies using the heterologous expression systems Saccharomyces cerevisiae and Xenopus laevis oocytes indicated that TaHKT1;5‐D is a Na⁺‐selective transporter. Transient expression in Arabidopsis thaliana mesophyll protoplasts and in situ polymerase chain reaction indicated that TaHKT1;5‐D is localised on the plasma membrane in the wheat root stele. RNA interference‐induced silencing decreased the expression of TaHKT1;5‐D in transgenic bread wheat lines which led to an increase in the Na⁺ concentration in the leaves. This indicates that TaHKT1;5‐D retrieves Na⁺ from the xylem vessels in the root and has an important role in restricting the transport of Na⁺ from the root to the leaves in bread wheat. Thus, TaHKT1;5‐D confers the essential salinity tolerance mechanism in bread wheat associated with the Kna1 locus via shoot Na⁺ exclusion and is critical in maintaining a high K⁺/Na⁺ ratio in the leaves. These findings show there is potential to increase the salinity tolerance of bread wheat by manipulation of HKT1;5 genes.