Soil salinity is one of the major environmental stresses affecting crop production worldwide, costing over $27Bln per year in lost opportunities to agricultural sector and making improved salinity tolerance of crops a critical step for sustainable food production. Salicylic acid (SA) is a signalling molecule known to participate in defence responses against variety of environmental stresses including salinity. However, the specific knowledge on how SA signalling propagates and promotes salt tolerance in plants remains largely unknown. This review focuses on the role of SA in regulation of ion transport processes during salt stress. In doing this, we briefly summarise a current knowledge on SA biosynthesis and metabolism, and then discuss molecular and physiological mechanisms mediating SA intracellular and long distance transport. We then discuss mechanisms of SA sensing and interaction with other plant hormones and signalling molecules such as ROS, and how this signalling affects activity of sodium and potassium transporters during salt stress. We argue that NPR1mediated SA signalling is pivotal for (i) controlling Na + entry into roots and the subsequent long-distance transport into shoots, (ii) enhancing H +-ATPase activity in roots, (iii) preventing stress-induced K + leakage from roots via depolarisation-activated potassium outward-rectifying channel (KOR) and ROS-activated non-selective cation channels (NSCC), and (iv) increasing K + concentration in shoots during salt stress. Future work should focus on how SA can regulate Na + exclusion and sequestration mechanisms in plants.
Despite numerous reports implicating salicylic acid (SA) in plant salinity responses, the specific ionic mechanisms of SA-mediated adaptation to salt stress remain elusive. To address this issue, a non-invasive microelectrode ion flux estimation technique was used to study kinetics of NaCl-induced net ion fluxes in Arabidopsis thaliana in response to various SA concentrations and incubation times. NaCl-induced K+ efflux and H+ influx from the mature root zone were both significantly decreased in roots pretreated with 10–500 μM SA, with strongest effect being observed in the 10–50 μM SA range. Considering temporal dynamics (0–8-h SA pretreatment), the 1-h pretreatment was most effective in enhancing K+ retention in the cytosol. The pharmacological, membrane potential, and shoot K+ and Na+ accumulation data were all consistent with the model in which the SA pretreatment enhanced activity of H+-ATPase, decreased NaCl-induced membrane depolarization, and minimized NaCl-induced K+ leakage from the cell within the first hour of salt stress. In long-term treatments, SA increased shoot K+ and decreased shoot Na+ accumulation. The short-term NaCl-induced K+ efflux was smallest in the gork1-1 mutant, followed by the rbohD mutant, and was highest in the wild type. Most significantly, the SA pretreatment decreased the NaCl-induced K+ efflux from rbohD and the wild type to the level of gork1-1, whereas no effect was observed in gork1-1. These data provide the first direct evidence that the SA pretreatment ameliorates salinity stress by counteracting NaCl-induced membrane depolarization and by decreasing K+ efflux via GORK channels.
Magnesium is pivotal for activating a large number of enzymes; hence, magnesium plays an important role in numerous physiological and biochemical processes affecting plant growth and development. Magnesium can also ameliorate aluminium phytotoxicity, but literature reports on the dynamics of magnesium homeostasis upon exposure to aluminium are rare. Herein existing knowledge on the magnesium transport mechanisms and homeostasis maintenance in plant cells is critically reviewed. Even though overexpression of magnesium transporters can alleviate aluminium toxicity in plants, the mechanisms governing such alleviation remain obscure. Possible magnesium-dependent mechanisms include (i) better carbon partitioning from shoots to roots; (ii) increased synthesis and exudation of organic acid anions; (iii) enhanced acid phosphatase activity; (iv) maintenance of proton-ATPase activity and cytoplasmic pH regulation; (v) protection against an aluminium-induced cytosolic calcium increase; and (vi) protection against reactive oxygen species. Future research should concentrate on assessing aluminium toxicity and tolerance in plants with overexpressed or antisense magnesium transporters to increase understanding of the aluminium-magnesium interaction.
Ion flux kinetics associated with blue light (BL) treatment of two wild types (WTs) and the phot1, phot2 and phot1͞phot2 mutants of Arabidopsis were studied by using the MIFE noninvasive ionselective microelectrode technique. BL induced significant changes in activity of H ؉ and Ca 2؉ transporters within the first 10 min of BL onset, peaking between 3 and 5 min. In all WT plants and in phot2 mutants, BL induced immediate Ca 2؉ influx. In phot1 and phot1͞ phot2 mutants, net Ca 2؉ flux remained steady. It is suggested that PHOT1 regulates Ca 2؉ uptake into the cytoplasm from the apoplast. Changes in ion fluxes were measured from cotyledons of intact seedlings and from the cut top of the hypocotyl of decapitated seedlings. Thus the photoreceptors mediating BL-induced Ca 2؉ and H ؉ fluxes are present in the rest of the decapitated seedling and probably in the cotyledons as well. The H ؉ and Ca 2؉ flux responses to BL appear not to be linked because, (i) when changes were observed for both ions, Ca 2؉ flux changed almost immediately, whereas H ؉ flux lagged by about 1.5 min; (ii) in the Wassilewskija ecotype, changes in H ؉ fluxes were small. Finally, wave-like changes in Ca 2؉ and H ؉ concentrations were observed along the cotyledon-hook axis regardless of its orientation to the light. Blue light (BL) is a key factor controlling plant growth and morphogenesis. Among numerous physiological processes controlled by BL are phototropism (bending toward or away from the light source), cotyledon expansion, and inhibition of hypocotyl elongation (1-3). These reactions are preceded or accompanied by significant changes in electrochemical properties of cells and tissues, including changes in membrane potential and ion transport across membranes (4-6).For more than 60 years, the interpretation of the multiphasic transient surface electrical responses of plants to light (7-11) was problematic and speculative (4). More recently, with microelectrode impalements, those responses have been located at the plasma membrane (12, 13), and it is now possible to interpret them in terms of specific ionic movements (5). BL induces transient extracellular acidification of epidermal cells of young pea leaves (14, 15). This acidification was found to be linked to Ca 2ϩ entry and Ca 2ϩ -calmodulin binding (14). BL also induces opening of anion (16) Unfortunately, there are pitfalls in inferring causal links between electrophysiological changes and BL-induced morphogenetic responses, based only on the similarity of the time scales of the measured responses. From their time scale, the photomorphogenetic reactions could be divided into several groups. The quickest observed (within minutes) are reactions associated with inhibition of hypocotyl elongation (11, 13). Next are bending responses, operating within the time scale of hours. The slowest are reactions of cotyledon expansion, which take days (2). However, it is quite possible that all these reactions may be induced simultaneously (moreover, they could be linked), and the observed difference ...
SummaryNPR1-dependent salicylic acid signalling controls sodium entry into the roots while preventing potassium loss through depolarization-activated outward-rectifying potassium and ROS-activated non-selective cation channels during salt and oxidative stresses.
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