Salinity is a major abiotic stress affecting approximately 7% of the world's total land area resulting in billion dollar losses in crop production around the globe. Recent progress in molecular genetics and plant electrophysiology suggests that the ability of a plant to maintain a high cytosolic K+/Na+ ratio appears to be critical to plant salt tolerance. So far, the major efforts of plant breeders have been aimed at improving this ratio by minimizing Na+ uptake and transport to shoot. In this paper, we discuss an alternative approach, reviewing the molecular and ionic mechanisms contributing to potassium homeostasis in salinized plant tissues and discussing prospects for breeding for salt tolerance by targeting this trait. Major K+ transporters and their functional expression under saline conditions are reviewed and the multiple modes of their control are evaluated, including ameliorative effects of compatible solutes, polyamines and supplemental calcium. Subsequently, the genetic aspects of inheritance of K+ transport 'markers' are discussed in the general context of salt tolerance as a polygenic trait. The molecular identity of 'salt tolerance' genes is analysed, and prospects for future research and breeding are examined.

Halophytes are defined as plants that are adapted to live in soils containing high concentrations of salt and benefiting from it, and thus represent an ideal model to understand complex physiological and genetic mechanisms of salinity stress tolerance. It is also known that oxidative stress signalling and reactive oxygen species (ROS) detoxification are both essential components of salinity stress tolerance mechanisms. This paper comprehensively reviews the differences in ROS homeostasis between halophytes and glycophytes in an attempt to answer the questions of whether stress-induced ROS production is similar between halophytes and glycophytes; is the superior salinity tolerance in halophytes attributed to higher antioxidant activity; and is there something special about the specific 'pool' of enzymatic and non-enzymatic antioxidants in halophytes. We argue that truly salt-tolerant species possessing efficient mechanisms for Na(+) exclusion from the cytosol may not require a high level of antioxidant activity, as they simply do not allow excessive ROS production in the first instance. We also suggest that H2O2 'signatures' may operate in plant signalling networks, in addition to well-known cytosolic calcium 'signatures'. According to the suggested concept, the intrinsically higher superoxide dismutase (SOD) levels in halophytes are required for rapid induction of the H2O2 'signature', and to trigger a cascade of adaptive responses (both genetic and physiological), while the role of other enzymatic antioxidants may be in decreasing the basal levels of H2O2, once the signalling has been processed. Finally, we emphasize the importance of non-enzymatic antioxidants as the only effective means to prevent detrimental effects of hydroxyl radicals on cellular structures.

This review argues that learning from halophytes may be a promising way of achieving this goal. The paper is focused around two central questions: what are the key physiological mechanisms conferring salinity tolerance in halophytes that can be introduced into non-halophyte crop species to improve their performance under saline conditions and what specific genes need to be targeted to achieve this goal? The specific traits that are discussed and advocated include: manipulation of trichome shape, size and density to enable their use for external Na(+) sequestration; increasing the efficiency of internal Na(+) sequestration in vacuoles by the orchestrated regulation of tonoplast NHX exchangers and slow and fast vacuolar channels, combined with greater cytosolic K(+) retention; controlling stomata aperture and optimizing water use efficiency by reducing stomatal density; and efficient control of xylem ion loading, enabling rapid shoot osmotic adjustment while preventing prolonged Na(+) transport to the shoot.

Regulation of the trans-plasma membrane pH gradient is an important part of plant responses to several hormonal and environmental cues, including auxin, blue light, and fungal elicitors. However, little is known about the signaling components that mediate this regulation. Here, we report that an Arabidopsis thaliana Ser/Thr protein kinase, PKS5, is a negative regulator of the plasma membrane proton pump (PM H+ -ATPase). Loss-of-function pks5 mutant plants are more tolerant of high external pH due to extrusion of protons to the extracellular space. PKS5 phosphorylates the PM H+ -ATPase AHA2 at a novel site, Ser-931, in the C-terminal regulatory domain. Phosphorylation at this site inhibits interaction between the PM H+ -ATPase and an activating 14-3-3 protein in a yeast expression system. We show that PKS5 interacts with the calcium binding protein SCaBP1 and that high external pH can trigger an increase in the concentration of cytosolic-free calcium. These results suggest that PKS5 is part of a calcium-signaling pathway mediating PM H+ -ATPase regulation.

SummaryReactive oxygen species (ROS) are central to plant stress response, signalling, development and a multitude of other processes. In this study, the plasma-membrane hydroxyl radical (HR)-activated K + channel responsible for K + efflux from root cells during stress accompanied by ROS generation is characterised. The channel showed 16-pS unitary conductance and was sensitive to Ca 2+ , tetraethylammonium, Ba 2+ , Cs + and free-radical scavengers. The channel was not found in the gork1-1 mutant, which lacks a major plasma-membrane outwardly rectifying K + channel. In intact Arabidopsis roots, both HRs and stress induced a dramatic K + efflux that was much smaller in gork1-1 plants. Tests with electron paramagnetic resonance spectroscopy showed that NaCl can stimulate HR generation in roots and this might lead to K + -channel activation. In animals, activation of K + -efflux channels by HRs can trigger programmed cell death (PCD). PCD symptoms in Arabidopsis roots developed much more slowly in gork1-1 and wild-type plants treated with K + -channel blockers or HR scavengers. Therefore, similar to animal counterparts, plant HR-activated K + channels are also involved in PCD. Overall, this study provides new insight into the regulation of plant cation transport by ROS and demonstrates possible physiological properties of plant HR-activated K + channels.