Na+ and water fluxes across cell membranes of the freshwater cyanobacterium Synechococcus as reported by chlorophyll a fluorescence Na+ and water fluxes across cell membranes of the freshwater cyanobacterium Synechococcus as reported by chlorophyll a flu

Abstract

During a salinity upshock episode cells of freshwater cyanobacterium Synechococcus undergo transient changes in the osmotic volume (¿VOSM), and the intensity of phycobilisome-sensitized chlorophyll a (Chla) fluorescence (¿FOSM), with ¿FOSM µ VOSM [Stamatakis K, Ladas NP, Alygizaki-Zorba A, Papageorgiou GC Arch. Biochem. Biophys. 370 (1999) 240-249]. Within 2-3 min, a jump of ¿[¿aCl] = 0.4 M drives Chla fluorescence and cell volume to maximum (VMAX, FMAX; rise branch), and then within 50-60 min to a lower end level (VT, FT; decay branch). The rise branch is dominated by passive influx of Na+, Cl-, and water; the ensuing decay branch by active extrusion of Na+ ions. The rise of Chla fluorescence comprises two consecutive first order processes (typical half-rise times ¿1 = 5 s and ¿1 = 23 s), it is not affected by water channel blockers (HgCl2, organic mercurials), nor by voltage gated Na+ channel blockers (phenytoin, lidocaine), but accelerated by protonophores and alkaline pH. The rise rate of Chla fluorescence appears to be determined by the uptake of Na+ and Cl- (passive co-transport), and not by the osmotic influx of water. At pH 6.5, the fluorescence decay branch (¿3 » 12 ¿ 15 min) is slowed by protonophores (CCCP), but not by voltage-gated Na+ channel blockers. At pH 9.0, it is slowed by vanadate ions (Na+-ATPase inhibitors) and by light starvation of the cells. We interpret these results as indicating extrusion of Na+ by Synechococcus cells via both primary (Na+-ATPases) and secondary (Na+/H+ antiporters) active transport processes. Supported by the Gen. Sec. Research. & Technology, Greece (PENED/99ED227).