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Applied and Environmental Microbiology, August 2005, p. 4531-4538, Vol. 71, No. 8
0099-2240/05/$08.00+0 doi:10.1128/AEM.71.8.4531-4538.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Swammerdam Institute of Life Sciences, Department of Molecular Microbial Physiology, University of Amsterdam, Nieuwe Achtergracht 166, 1018 WV Amsterdam, The Netherlands,1 Swammerdam Institute of Life Sciences, Dept. Molecular Biology & Microbial Food Safety, University of Amsterdam, Nieuwe Achtergracht 166, 1018 WV Amsterdam, The Netherlands,2 Unilever Research & Development, Olivier van Noortlaan 120, 3133 AT Vlaardingen, The Netherlands3
Received 20 October 2004/ Accepted 14 March 2005
This paper reports on physiological and molecular responses of Saccharomyces cerevisiae to heat stress conditions. We observed that within a very narrow range of culture temperatures, a shift from exponential growth to growth arrest and ultimately to cell death occurred. A detailed analysis was carried out of the accumulation of trehalose and the activation of the protein kinase C1 (PKC1) (cell integrity) pathway in both glucose- and ethanol-grown cells upon temperature upshifts within this narrow range of growth temperatures. It was observed that the PKC1 pathway was hardly activated in a tps1 mutant that is unable to accumulate any trehalose. Furthermore, it was observed that an increase of the extracellular osmolarity during a continuous heat stress prevented the activation of the pathway. The results of these analyses support our hypothesis that under heat stress conditions the activation of the PKC1 pathway is triggered by an increase in intracellular osmolarity, due to the accumulation of trehalose, rather than by the increase in temperature as such.
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