Osmotic Stress Signaling and Osmoadaptation in Yeasts
Abstract
The ability to adapt to altered availability of free water is a fundamental property of living cells. The principles underlying osmoadaptation are well conserved. The yeast Saccharomyces cerevisiae is an excellent model system with which to study the molecular biology and physiology of osmoadaptation. Upon a shift to high osmolarity, yeast cells rapidly stimulate a mitogen-activated protein (MAP) kinase cascade, the high-osmolarity glycerol (HOG) pathway, which orchestrates part of the transcriptional response. The dynamic operation of the HOG pathway has been well studied, and similar osmosensing pathways exist in other eukaryotes. Protein kinase A, which seems to mediate a response to diverse stress conditions, is also involved in the transcriptional response program. Expression changes after a shift to high osmolarity aim at adjusting metabolism and the production of cellular protectants. Accumulation of the osmolyte glycerol, which is also controlled by altering transmembrane glycerol transport, is of central importance. Upon a shift from high to low osmolarity, yeast cells stimulate a different MAP kinase cascade, the cell integrity pathway. The transcriptional program upon hypo-osmotic shock seems to aim at adjusting cell surface properties. Rapid export of glycerol is an important event in adaptation to low osmolarity. Osmoadaptation, adjustment of cell surface properties, and the control of cell morphogenesis, growth, and proliferation are highly coordinated processes. The Skn7p response regulator may be involved in coordinating these events. An integrated understanding of osmoadaptation requires not only knowledge of the function of many uncharacterized genes but also further insight into the time line of events, their interdependence, their dynamics, and their spatial organization as well as the importance of subtle effects.
Acknowledgments
I thank the many colleagues, especially L. Adler, G. Ammerer, A. Blomberg, J. Fassler, J. Labarre, M. Proft, F. Posas, B. A. Prior, and P. Sunnerhagen, who shared data and discussed their interpretation. Special thanks go to A. Gasch for help with the interpretation of microarray data and the members of my group for many discussions and patience during preparation of the manuscript. I apologize to those who might feel that their work was not adequately taken into account.
I am a special researcher (särkild forskare) supported by the Swedish Research Council. Work in my laboratory is supported by grants from the Swedish Research Council, Formas (the Swedish Research Council for Environment, Agricultural Sciences and Spatial Planning), several contracts with the European Commission, and the Human Frontier Science Organization.
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