A glimpse of the mechanisms of ion homeostasis during salt stress

Abstract

Cells respond to salt stress by osmolyte synthesis and by increase of K+ uptake and Na+ efflux at the plasma membrane and of Na+ accumulation at the vacuole. This cellular level of response has been approached by the molecular genetics of Saccharomyces cerevisiae. Two plasma membrane proteins, Sln1 and Sho1, operate as sensors for turgor loss under mild osmotic stress. They activate the Hog1 MAP kinase which induces several defence genes, including the ENA1 Na+-efflux pump. Hog1-mediated induction occurs by inactivation of the Sko1 repressor. High concentrations of Na+ activate the calcium-dependent protein phosphatase calcineurin, which induces the ENA1 gene via the positive transcription factor Hal8/Crz1/Tcn1. Vacuoles could operate as Na+ sensors through a Na+-Ca2+ exchange mechanism. The electrical potential of the plasma membrane is a major determinant of the uptake of toxic cations, including Na+, by non-specific leakage pathways. This biophysical parameter is modulated by the concerted activities of the proton pumping Pma1 ATPase and the Trk1,2 K+ uptake system. Both calcineurin and the protein kinase Hal4,5 modulate Trk1,2 and, indirectly, the membrane potential and salt tolerance. The limiting role of vacuolar cation accumulation in salt tolerance has been demonstrated by expression in yeast vacuoles of the bacterial antiporter NhaA.