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Stabilization of two families of critical targets for hyperthermic cell killing and acquired thermotolerance of yeast cells
Author(s) -
Obuchi Kaoru,
Iwahashi Hitoshi,
Lepock James R.,
Komatsu Yasuhiko
Publication year - 1998
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/(sici)1097-0061(1998100)14:14<1249::aid-yea323>3.0.co;2-a
Subject(s) - biology , yeast , saccharomyces cerevisiae , phase (matter) , shock (circulatory) , microbiology and biotechnology , programmed cell death , arrhenius equation , heat shock , biophysics , heat shock protein , exponential growth , genetics , gene , apoptosis , kinetics , chemistry , physics , medicine , organic chemistry , quantum mechanics
Hyperthermic cell killing profiles of Saccharomyces cerevisiae cells were biphasic and a shoulder (phase 1) was followed by an exponential killing (phase 2). Assuming that (i) the rate of thermal damage in particular macromolecules or their assemblies limits the rate of hyperthermic cell killing (the critical target model), and (ii) the damages of two families of targets are lethal independently, we built a ‘dual critical target model’ in order to interpret the biphasic cell killing. Time‐courses of temperature‐programmed fractional survival were traced for S. cerevisiae cells in exponentially growing phase, heat shocked, and in stationary phase. Non‐linear curve‐fitting of the time‐courses by using the dual critial target model provided the Arrhenius parameters of denaturation of the two families of targets. The cells were killed more slowly in phase 1 than in phase 2. Arrest in stationary phase, not heat shock, stabilizes the family of targets that is critical to phase 1 death. On the other hand, both heat‐shock response and arrest in stationary phase stabilizes the other family of targets that, in addition to the previous one, is responsible for phase 2 death. © 1998 John Wiley & Sons, Ltd.