Mechanisms underlying turgor regulation in the estuarine alga V aucheria erythrospora ( X anthophyceae) exposed to hyperosmotic shock

Aquatic organisms are often exposed to dramatic changes in salinity in the environment. Despite decades of research, many questions related to molecular and physiological mechanisms mediating sensing and adaptation to salinity stress remain unanswered. Here, responses of V aucheria erythrospora , a turgor‐regulating xanthophycean alga from an estuarine habitat, have been investigated. The role of ion uptake in turgor regulation was studied using a single cell pressure probe, microelectrode ion flux estimation ( MIFE ) technique and membrane potential ( E m ) measurements. Turgor recovery was inhibited by G d 3+ , tetraethylammonium chloride (TEA ), verapamil and orthovanadate. A N a C l‐induced shock rapidly depolarized the plasma membrane while an isotonic sorbitol treatment hyperpolarized it. Turgor recovery was critically dependent on the presence of N a + but not K + and C l − in the incubation media. Na + uptake was strongly decreased by amiloride and changes in net N a + and H + fluxes were oppositely directed. This suggests active uptake of N a + in V . erythrospora mediated by an antiport N a + / H + system, functioning in the direction opposite to that of the SOS 1 exchanger in higher plants. The alga also retains K + efficiently when exposed to high N a C l concentrations. Overall, this study provides insights into mechanisms enabling V . erythrospora to regulate turgor via ion movements during hyperosmotic stress.