INTRACELLULAR NA+ AND K+ CONTENTS OF ZYGOSACCHAROMYCES-ROUXII MUTANTS DEFECTIVE IN SALT TOLERANCE

Two of five Zygosaccharomyces rouxil mutants defective in salt tolerance, 152S (sat1) and 1717S (SAT3), were inviable in a nutrient medium (YPD) containing more than 1% NaCl. These two mutant cells contained significantly higher amounts of Na+ (298-mu-mol and 285-mu-mol per g cells of 152S and 1717S, respectively) but lower amounts of K+ (242-mu-mol and 176-mu-mol per g cells of 152S and 1717S, respectively) than three other mutants, 41S (sat2-1 [98-mu-mol Na+ and 326-mu-mol K+/g cells]), 197S (sat2-2 [103-mu-mol Na+ and 336-mu-mol K+/g cells]), 1611S (SAT4 [139-mu-mol Na+ and 294-mu-mol K+/g cells]), as well as a wild-type strain, AN39 (61-mu-mol Na+ and 349-mu-mol K+/g cells), when cultured in YPD medium containing 0.8% NaCl. A KCI supplement, optimally 0.6 M, added to the medium somewhat restored the NaCl-hypersensitivity of 152S and 1717S with a concomitant decrease of intracellular Na+. This finding suggests that the NaCl-hypersensitive mutations are due to a defect in the Na+-regulating mechanism. The other three mutants showed weak responses to KCl in high NaCl-YPD. These five salt sensitive mutants and the wild-type strain retained the same levels of intracellular glycerol and arabitol when transferred into NaCl (5%)-YPD from YPD medium. This suggests that polyol accumulation is not the only mechanism of salt tolerance in Z. rouxii.