ENERGY-METABOLISM OF CANDIDA (YARROWIA) LIPOLYTICA YEAST UNDER NONSTRESS AND SALINITY STRESS CONDITIONS

The effect of a high (9%) NaCl concentration in the nutrient medium on the growth and energy metabolism of the halotolerant yeast Candida (Y arrowia) lipolytica (Wick.) Van der Walt and Arx. was investigated. Th e yeast cells readily utilized hexoses, organic acids (succinate, acet ate, and citrate), ethanol, and glycerol as sole sources of carbon and energy, Oxygen consumption by intact cells was mediated by two termin al oxidases, i.e., the cytochrome oxidase and the alternative oxidase, albeit to varying extents at different growth phases, with the greate r participation of the alternative pathway upon reaching the stationar y growth phase. The capacity of cells to grow on succinate (which is u tilized exclusively through the main respiratory chain), as well as th e observation that micromolar concentrations of ethidium bromide (an i nhibitor of mitochondrial transcription) almost totally inhibited cell growth on both fermentable and nonfermentable substrates, suggests th at the oxidative phosphorylation system plays an important, if not exc lusive, role in the cell energy budget of this yeast strain, The oxida tive phosphorylation system was not accessible to glucose repression. Mitochondria isolated from the yeast cells grown under normal conditio ns displayed respiratory and phosphorylative activities, indicating a respiratory chain with three points of energy conservation. Salinity s tress (9% NaCl) resulted in diminished (by two to three times) growth rates (when cells utilized sucrose, ethanol, or glycerol), a complete loss of capacity to utilize succinate, and enhanced respiration resist ant to cyanide, As can be inferred from the analysis of oxidative and phosphorylating activities of mitochondria, salinity stress was accomp anied by pronounced changes in the organization of the respiratory cha in, including a delayed expression of the alternative oxidase, lower r ates of the oxidation of NAD-linked substrates, and dramatically incre ased compensatory activity of succinate oxidase. The mechanisms underl ying the halotolerance of yeast cells are discussed.