TL;DR: An evolutionarily conserved mitogen-activated protein kinase pathway--the high osmolarity glycerol (HOG) pathway--mediates the hyperosmotic response in Saccharomyces cerevisiae.
TL;DR: It is shown that knockout (KO) and overexpression (OE) of previously uncharacterized PLD α3 alter plant response to salinity and water deficit and that increased PLDα3 expression and associated lipid changes promote root growth, flowering, and stress avoidance.
Abstract: Rapid activation of phospholipase D (PLD), which hydrolyzes membrane lipids to generate phosphatidic acid (PA), occurs under various hyperosmotic conditions, including salinity and water deficiency. The Arabidopsis thaliana PLD family has 12 members, and the function of PLD activation in hyperosmotic stress responses has remained elusive. Here, we show that knockout (KO) and overexpression (OE) of previously uncharacterized PLDα3 alter plant response to salinity and water deficit. PLDα3 uses multiple phospholipids as substrates with distinguishable preferences, and alterations of PLDα3 result in changes in PA level and membrane lipid composition. PLDα3-KO plants display increased sensitivities to salinity and water deficiency and also tend to induce abscisic acid–responsive genes more readily than wild-type plants, whereas PLDα3-OE plants have decreased sensitivities. In addition, PLDα3-KO plants flower later than wild-type plants in slightly dry conditions, whereas PLDα3-OE plants flower earlier. These data suggest that PLDα3 positively mediates plant responses to hyperosmotic stresses and that increased PLDα3 expression and associated lipid changes promote root growth, flowering, and stress avoidance.
TL;DR: This work functionally defined the smallest sequence able to confer hyperosmotic response on a downstream gene independent of other putative cis-elements, that is, a minimal essential osmotic response element (ORE).
TL;DR: It is concluded that the rapid signal for adaptation to higher salinities is an increased tonicity of the plasma that induces chloride cell shrinkage, increased chloride secretion with activation of the Na+K+2Cl− cotransporter, theNa+/H+ exchanger and opening of Cl− channels.
Abstract: Transition from low salt water to sea water of the euryhaline fish, Fundulus heteroclitus, involves a rapid signal that induces salt secretion by the gill chloride cells. An increase of 65 mOsm in plasma osmolarity was found during the transition. The isolated, chloridecell-rich opercular epithelium of sea-water-adapted Fundulus exposed to 50 mOsm mannitol on the basolateral side showed a 100% increase in chloride secretion, which was inhibited by bumetanide 10−4
m and 10−4
m DPC (N-Phenylanthranilic acid). No effect of these drugs was found on apical side exposure. A Na+/H+ exchanger, demonstrated by NH4Cl exposure, was inhibited by amiloride and its analogues and stimulated by IBMX, phorbol esters, and epithelial growth factor (EGF). Inhibition of the Na+/H+ exchanger blocks the chloride secretion increase due to basolateral hypertonicity. A Cl−/HCO
3
−
exchanger was also found in the chloride cells, inhibited by 10−4
m DIDS but not involved in the hyperosmotic response. Ca2+ concentration in the medium was critical for the stimulation of Cl− secretion to occur. Chloride cell volume shrinks in response to hypertonicity of the basolateral side in sea-water-adapted operculi; no effect was found on the apical side. Freshwater-adapted fish chloride cells show increased water permeability of the apical side. It is concluded that the rapid signal for adaptation to higher salinities is an increased tonicity of the plasma that induces chloride cell shrinkage, increased chloride secretion with activation of the Na+K+2Cl− cotransporter, the Na+/H+ exchanger and opening of Cl− channels.
TL;DR: The TS and its associated transport activity represent essential components of a recently proposed paracellular transport model for chloride cells and the TS of the pseudobranch cell is discussed in this review.
Abstract: Chloride cells represent the sites of branchial osmoregulatory activity of teleosts. The cells undergo characteristic changes with osmotic challenge and the response is mediated by hormones. Either increased salinity or cortisol treatment will elicit well-known changes in chloride cells; these changes are clearly interrelated and may be collectively referred to as the "hyperosmotic response" of chloride cells. Fundamental features of the "hyperosmotic response" include proliferation and hypertrophy of chloride cells, an amplification of the cell's extensive tubular network or tubular system (TS), an increase in the specific activity of the transport-associated enzyme, Na-K-ATPase, and a concomitant increase in electrolyte transport. The TS displays frequent examples of continuity with the basolateral plasmalemma and the Na-K-ATPase enzyme complex resides in the membranes of the TS. The enzyme complex maintains its conventional polarity with regard to internal substrate and sodium binding sites and external or TS luminal surface, potassium, and ouabain binding sites. The luminal surface of the TS is anionic at pH 1.8 and above. The TS membranes display in situ, in isolation, and by freeze fracture, a characteristic asymmetric structure consisting of repeating particles; larger particles are associated with the cytoplasmic surface of the membrane and smaller particles with the external or luminal surface of tubules. The dimensions of the particles, and their disposition with respect to the cytoplasmic and external surfaces of the TS membrane, support the hypothesis that they are the visual manifestation of the transport-associated Na-K-ATPase complex. The TS and its associated transport activity represent essential components of a recently proposed paracellular transport model for chloride cells. The TS of the pseudobranch cell is also discussed in this review.