A glimpse of the mechanisms of ion homeostasis during salt stress

Cells respond to salt stress by osmolyte synthesis and by increase of K+ up take and Na+ efflux at the plasma membrane and of Na+ accumulation at the v acuole. This cellular level of response has been approached by the molecula r genetics of Saccharomyces cerevisiae. Two plasma membrane proteins, SIn1 and Sho1, operate as sensors for turgor loss under mild osmotic stress, The y activate the Hog1 MAP kinase which induces several defence genes, includi ng the ENA1 Na+-efflux pump. Hog1-mediated induction occurs by inactivation of the Sko1 repressor. High concentrations of Na+ activate the calcium-dep endent protein phosphatase calcineurin, which induces the ENA1 gene via the positive transcription factor HaI8/Crz1/Tcn1. Vacuoles could operate as Na + sensors through a Na+-Ca2+ exchange mechanism, The electrical potential o f the plasma membrane is a major determinant of the uptake of toxic cations , including Na+, by non-specific leakage pathways. This biophysical paramet er is modulated by the concerted activities of the proton pumping Pma1 ATPa se and the Trk1,2 K+ uptake system. Both calcineurin and the protein kinase HaI4,5 modulate Trk1,2 and, indirectly, the membrane potential and salt to lerance. The limiting role of vacuolar cation accumulation in salt toleranc e has been demonstrated by expression in yeast vacuoles of the bacterial an tiporter NhaA.