Ion Transporters and Abiotic Stress Tolerance in Plants

Adaptation of plants to salt stress requires cellular ion homeostasis involving net intracellular Na+ and Cl− uptake and subsequent vacuolar compartmentalization without toxic ion accumulation in the cytosol. Sodium ions can enter the cell through several low- and high-affinity K+ carriers. Some members of the HKT family function as sodium transporter and contribute to Na+ removal from the ascending xylem sap and recirculation from the leaves to the roots via the phloem vasculature. Na+ sequestration into the vacuole depends on expression and activity of Na+/H+ antiporter that is driven by electrochemical gradient of protons generated by the vacuolar H+-ATPase and the H+-pyrophosphatase. Sodium extrusion at the root-soil interface is presumed to be of critical importance for the salt tolerance. Thus, a very rapid efflux of Na+ from roots must occur to control net rates of influx. The Na+/H+ antiporter SOS1 localized to the plasma membrane is the only Na+ efflux protein from plants characterized so far. In this paper, we analyze available data related to ion transporters and plant abiotic stress responses in order to enhance our understanding about how salinity and other abiotic stresses affect the most fundamental processes of cellular function which have a substantial impact on plant growth development.

Influences of Bentonite Modification Methods on the Physical and Chemical Properties of Bentonite

The current study focuses on the artificial modification of natural bentonite using pulping sodium, stacking sodium, extrusion sodium, wheel rolling sodium, and microwave sodium treatments. The effects of these methods on the physical and chemical properties of bentonite are investigated. The results indicate that the wheel rolling sodium treatment, which features the effects of extrusion and kneading, facilitated maximum separation and sodium treatment of Ca2+and Mg2+in the lattice of bentonite. This method produced highly efficient Ca-bentonite with full modification. When the wheel rolling sodium treatment was performed for 60 min, the modified bentonite exhibited a colloid index of 300 mL/3 g, swelling value of 275 mL/2 g, swelling volume of 94 mL/g, and 2 h water absorption of 755%. The modified bentonite has desirable cohesiveness, dilatability, suspension property, dispersibility, and high physical and chemical performances, which are suitable for use as iron ore concentrate pallet and casting bentonite binders.

Erythrocyte enzymopathies

Numerous enzymes, including those of the hexose monophosphate pathway and glycolysis, are active in the red cell. They are required for the generation of ATP (needed to supply energy for sodium extrusion) and the reductants NADH and NADPH, necessary to maintain haemoglobin in its active ferrous atomic state, as well as for the integrity of sulphydryl groups present on essential proteins. 2,3-diphosphoglycerate (2,3-DPG), an intermediate of ...

Regulation of ENA1 Na+-ATPase Gene Expression by the Ppz1 Protein Phosphatase Is Mediated by the Calcineurin Pathway

ABSTRACT Saccharomyces cerevisiae strains lacking the Ppz1 protein phosphatase are salt tolerant and display increased expression of the ENA1 Na+-ATPase gene, a major determinant for sodium extrusion, while cells devoid of the similar Ppz2 protein do not show these phenotypes. However, a ppz1 ppz2 mutant displays higher levels of ENA1 expression than the ppz1 strain. We show here that the increased activity of the ENA1 promoter in a ppz1 ppz2 mutant maps to two regions: one region located at −751 to −667, containing a calcineurin-dependent response element (CDRE), and one downstream region (−573 to −490) whose activity responds to intracellular alkalinization. In contrast, the increased ENA1 expression in a ppz1 mutant is mediated solely by an intact calcineurin/Crz1 signaling pathway, on the basis that (i) this effect maps to a single region that contains the CDRE and (ii) it is blocked by the calcineurin inhibitor FK506, as well as by deletion of the CNB1 or CRZ1 gene. The calcineurin dependence of the increased ENA1 expression of a ppz1 mutant would suggest that Ppz1 could negatively regulate calcineurin activity. In agreement with this notion, a ppz1 strain is calcium sensitive, and this mutation does not result in a decrease in the calcium hypertolerance of a cnb1 mutant. It has been shown that ENA1 can be induced by alkalinization of the medium and that a ppz1 ppz2 strain has a higher intracellular pH. However, we present several lines of evidence that show that the gene expression profile of a ppz1 mutant does not involve an alkalinization effect. In conclusion, we have identified a novel role for calcineurin, but not alkalinization, in the control of ENA1 expression in ppz1 mutants.

Electrophysiological correlates of fluid transport in cultured porcine thyroid cells

ABSTRACT Confluent monolayers of cultured porcine thyroid cells transport fluid from the apical to the basal surface, forming circumscribed zones of detachment from the culture dish substrate (domes). The transepithelial potential (TEP), positive on the basal side, was 12·9 ± 0·4 (s.e.m.) mV (n = 93) under control conditions, increasing to 38·9 ± 0·3 mV (n = 281) when fluid transport was stimulated by prostaglandin E2 (PGE2; 1 μmol/l). Forskolin (1 μmol/l) and 8-(4-chlorophenylthio) adenosine 3′,5′-cyclic monophosphate (0·5 mmol/l) were also effective in increasing TEP. Addition of amiloride in concentrations sufficient to block fluid transport (100 μmol/l) reduced the TEP to 5·8 ± 0·3 mV (n=76). Substitution of N-methyl-d-glucamine for sodium in the medium reduced the PGE2-stimulated TEP to 13·4 ± 0·8 mV (n = 32). Substitution of gluconate for chloride increased the TEP to 40·3 ± 0·4 mV (n = 160). Removal of bicarbonate or potassium from the medium, or addition of ouabain (200 μmol/l) were also effective in reducing the TEP. In media of low bicarbonate concentration (1 mmol NaHCO3/l), acetazolamide (1 mmol/l) reduced the TEP. Fluid transport by the monolayer as measured by the change in height of domes was increased by PGE2 (1 μmol/l). PGE2-stimulated fluid transport was inhibited by sodium or chloride ion substitution, bicarbonate removal or the addition of ouabain (200 μmol/l) or amiloride (100 μmol/l). It was concluded that fluid transport in thyroid monolayers is mediated by rheogenic sodium transport with chloride transport being passive, electrogenically coupled to sodium transport. Sodium entry to the apical pole of the cells occurs by an amiloride-sensitive mechanism, and sodium extrusion at the basal pole depends on the Na+/K+ ATPase. J. Endocr. (1988) 119, 309–314