Abstract
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. The protective effect was absent if cycloheximide was added immediately before heat exposure and the cells were incubated with the drug during the heat treatment and recovery period. The rate of ROS production and protective effect of cycloheximide on viability were significantly decreased in the case of severe (50°C) heat shock. Treatment with cycloheximide at 39°C inhibited the induction of Hsp104 synthesis and suppressed the development of induced thermotolerance to severe shock (50°C), but it had no effect on induced thermotolerance to moderate (45°C) heat shock. At the same time, Hsp104 effectively protected cells from death independently of the intensity of heat exposure. These data indicate that moderate heat shock induced programmed cell death in the yeast cells, and cycloheximide suppressed this process by inhibiting general synthesis of proteins.
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Abbreviations
- CFU:
-
colony-forming units
- DCF:
-
2′,7′-dichlo-rofluorescein
- Dnm1:
-
dynamin 1
- H2DCF·DA:
-
2′,7′-dichlorodihydrofluorescein diacetate
- Hsps:
-
heat shock proteins
- PCD:
-
programmed cell death
- ROS:
-
reactive oxygen species
- SDS:
-
sodium dodecyl sulfate
- Yca1 (MCA1):
-
yeast caspase 1
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Published in Russian in Biokhimiya, 2014, Vol. 79, No. 1, pp. 22–32.
Originally published in Biochemistry (Moscow) On-Line Papers in Press, as Manuscript BM13-232, November 24, 2013.
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Rikhvanov, E.G., Fedoseeva, I.V., Varakina, N.N. et al. Mechanism of Saccharomyces cerevisiae yeast cell death induced by heat shock. Effect of cycloheximide on thermotolerance. Biochemistry Moscow 79, 16–24 (2014). https://doi.org/10.1134/S0006297914010039
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DOI: https://doi.org/10.1134/S0006297914010039