MECHANISMS OF SALT TOLERANCE CONFERRED BY OVEREXPRESSION OF THE HAL1 GENE IN SACCHAROMYCES-CEREVISIAE

Overexpression of the HAL1 gene improves the tolerance of Saccharomyce s cerevisiae to NaCl by increasing intracellular K+ and decreasing int racellular Na+. The effect of HAL1 on intracellular Na+ was mediated b y the PMR2/ENA1 gene, corresponding to a major Na+ efflux system. The expression level of ENA1 was dependent on the gene dosage of HAL1 and overexpression of HAL1 suppressed the salt sensitivity of mil mutants in calcineurin and Hal3p, other known regulators of ENA1 expression. T he effect of HAL1 on intracellular K+ was independent of the TRK1 and TOK1 genes, corresponding to a major K+ uptake system and to a K+ effl ux system activated by depolarization, respectively. Overexpression of HAL1 reduces K+ loss from the cells upon salt stress: a phenomenon me diated by an unidentified K+ efflux system. Overexpression of HAL1 did not increase NaCl tolerance in galactose medium. NaCl poses two types of stress, osmotic and ionic, counteracted by glycerol synthesis and sodium extrusion, respectively. As compared to glucose, with galactose as carbon source glycerol synthesis is reduced and the expression of ENA1 is increased. As a consequence, osmotic adjustment through glycer olsynthesis, a process not affected by HAL1, is the limiting factor fo r growth on galactose under NaCl stress. (C) 1997 by John Wiley & Sons , Ltd.