The role of flavin-containing enzymes in mitochondrial membrane hyperpolarization and ROS production in respiring Saccharomyces cerevisiae cells under heat-shock conditions.

Heat shock is known to accelerate mitochondrial ROS production in Saccharomyces cerevisiae cells. But how yeast mitochondria produce ROS under heat-shock condition is not completely clear. Previously, it was shown that ROS production in heat-stressed fermenting yeast cells was accompanied by mitochondrial membrane potential (MMP) increase.

Relation between cell death progression, reactive oxygen species production and mitochondrial membrane potential in fermenting Saccharomyces cerevisiae cells under heat-shock conditions.

Moderate heat shock increased reactive oxygen species (ROS) production that led to cell death in glucose-grown Saccharomyces cerevisiae cells. Conditions that disturb mitochondrial functions such as treatment by uncouplers and petite mutation were shown to inhibit ROS production and protects cell from thermal death. Hence, mitochondria are responsible for ROS production and play an active role in cell death.

Heat shock induces production of reactive oxygen species and increases inner mitochondrial membrane potential in winter wheat cells.

Heat shock leads to oxidative stress. Excessive ROS (reactive oxygen species) accumulation could be responsible for expression of genes of heat-shock proteins or for cell death. It is known that in isolated mammalian mitochondria high protonic potential on the inner membrane actuates the production of ROS.

Mechanism of Saccharomyces cerevisiae yeast cell death induced by heat shock. Effect of cycloheximide on thermotolerance.

The mechanism of yeast cell death induced by heat shock was found to be dependent on the intensity of heat exposure. Moderate (45°C) heat shock strongly increased the generation of reactive oxygen species (ROS) and cell death. Pretreatment with cycloheximide (at 30°C) suppressed cell death, but produced no effect on ROS production.

Effect of amiodarone on thermotolerance and Hsp104p synthesis in the yeast Saccharomyces cerevisiae.

Amiodarone (AMD) is known to induce a transient increase in cytosolic Ca2+ level in cells of the yeast Saccharomyces cerevisiae. In the present study the effect of AMD on the thermotolerance and Hsp104p synthesis of the yeast was studied. AMD induced Hsp104p synthesis and increased survival of the yeast after a severe heat shock (50°C).

Chaperone effects on prion and nonprion aggregates.

Exposure to high temperature or other stresses induces a synthesis of heat shock proteins. Many of these proteins are molecular chaperones, and some of them help cells to cope with heat-induced denaturation and aggregation of other proteins. In the last decade, chaperones have received increased attention in connection with their role in maintenance and propagation of the Saccharomyces cerevisiae prions, infectious or heritable agents transmitted at the protein level.

Nuclear-mitochondrial cross-talk during heat shock in Arabidopsis cell culture.

Apart from energy generation, mitochondria perform a signalling function determining the life and death of a cell under stress exposure. In the present study we have explored patterns of heat-induced synthesis of Hsp101, Hsp70, Hsp17.6 (class I), Hsp17.

Do mitochondria regulate the heat-shock response in Saccharomyces cerevisiae?

A mild heat shock induces the synthesis of heat-shock proteins (hsps), which protect cells from damage during more extreme heat exposure. The nature of the signals that induce transcription of heat shock-regulated genes remains conjectural. In this work we studied the role of mitochondria in regulating hsps synthesis in Saccharomyces cerevisiae.

[Induction of synthesis of Hsp104 of Saccharomyces cerevisiae in heat shock is controlled by mitochondria].

Heat shock protein Hsp104 of Saccharomyces cerevisiae functions as a protector of cells against heat stress. When yeast are grown in media containing nonfermentable carbon sources, the constitutive level of this protein increases, which suggests an association between the expression of Hsp104 and yeast energy metabolism. In this work, it is shown that distortions in the function of mitochondria appearing as a result of mutation petite or after exposure of cells to the mitochondrial inhibitor sodium azide reduce the induction of Hsp104 synthesis during heat shock.

[The effect of sodium malonate on yeast thermotolerance].

The study of the effect of malonate (an inhibitor of the succinate dehydrogenase complex of the respiratory chain of mitochondria) on the thermotolerance of the fermentative Saccharomyces cerevisiae and nonfermentative Rhodotorula rubra yeasts showed that malonate augmented the damaging effect of heat shock on the yeasts utilizing glucose (or other sugars) by means of oxidative phosphorylation. At the same time, malonate did not influence and sometimes even improved the thermotolerance of the yeasts utilizing glucose through fermentation. The suggestion is made that cell tolerance to heat shock depends on the normal functioning of mitochondria.

[The absence of direct relationship between the ability of yeasts to grow at elevated temperatures and their survival after lethal heat shock].

The study of the growth of the yeasts Rhodotorula rubra, Saccharomyces cerevisiae, and Debaryomyces vanriji at elevated temperatures and their survival after transient lethal heat shock showed that the ability of these yeasts to grow at supraoptimal temperatures (i.e., their thermoresistance) and their ability to tolerate lethal heat shocks (i.

[Effect of cytochrome oxidase inhibitors on the yeast thermotolerance].

The investigation of the effect of the cytochrome oxidase inhibitors sodium cyanide and sodium azide on the thermotolerance of the yeasts Rhodotorula rubra, Debaryomyces vanriji, and Saccharomyces cerevisiae showed that these inhibitors diminish the thermotolerance of R. rubra and D. vanriji, but do not affect the thermotolerance of S.

[The effect of sodium azide on the thermotolerance of the yeast Saccharomyces cerevisiae and Candida albicans].

The addition of sodium azide (a mitochondrial inhibitor) at a concentration of 0.15 mM to glucosegrown Saccharomyces cerevisiae or Candida albicans cells before exposing them to heat shock increased cell survival. At higher concentrations of azide, its protective effect on glucose-grown cells decreased.

Sodium azide reduces the thermotolerance of respiratively grown yeasts.

The effect of sodium azide in heat shock-induced cell death was studied in Debaryomyces vanrijiae, Candida albicans, and Saccharomyces cerevisiae yeasts. The results presented demonstrate that the azide addition induced a drastic decrease in the thermotolerance of glucose-grown D. vanrijiae.

[Heat shock-induced changes in the respiration of the yeast Saccharomyces cerevisiae].

The incubation of Saccharomyces cerevisiae at elevated temperature (45 degrees C) stimulated the respiration of yeast cells and decreased their survival rate. The respiration-deficient mutant of this yeast was found to be more tolerant to the elevated temperature than the wild-type strain. At the same time, the cultivation of the wild-type strain in an ethanol-containing medium enhanced the respiration, catalase activity, and thermotolerance of yeast cells, as compared with their growth in a glucose-containing medium.

[Effect of sodium azide on heat-shock resistance in Saccharomyces cerevisiae and Debaryomyces vanriji yeasts].

The pretreatment of Saccharomyces cerevisiae and Debaryomyces vanriji with sodium azide was found to induce thermotolerance in both yeasts, whereas sodium azide used in combination with heat shock enhanced the thermotolerance of S. cerevisiae and substantially decreased the thermotolerance of D. vanriji.

Association of bacteria and yeasts in hot springs.

The thermophilic bacterium Bacillus sp. strain TB-1 was isolated in association with the yeast Debaryomyces vanriji from hot springs at 46 degrees C. It was shown that TB-1 excreted thiamine into the culture broth, which not only promoted D.