Turgor restoration : the critical event in signal cessation of the HOG pathway.
Bodil Nordlander (1), Peter Gennemark (2), Markus J Tamás (1), Sara Karlgren (1), Dag Wedelin (2), Stefan Hohmann (1)
(1) Cell and Molecular Biology, Göteborg University, Box 462, Göteborg, S-40530, Sweden;
(2) Computing Science, Chalmers University of Technology, Rännvägen 6B, 41296 Göteborg, Sweden
The activity of MAP kinase pathways is tightly controlled because kinase activity is required to elicit specific responses while prolonged activation is detrimental. We show that the critical event in deactivation of the osmosensing yeast HOG pathway is signal cessation. Inability to produce or to retain the osmolyte glycerol results in prolonged HOG pathway activation and enhanced expression of HOG target genes. Moreover, higher basal glycerol production results in faster glycerol accumulation and a reduced period of HOG pathway activation. Overproduction of a Hog1-deactivating protein phosphatase alters the amplitude but not the profile of pathway activation/deactivation. This observation is in accordance with a mathematical model. This model predicts that the HOG pathway can be reactivated by subsequent osmotic shock treatments provided its deactivation is controlled by signal cessation. In accordance with its role in turgor control, the HOG pathway indeed remains competent for further activation. To illustrate the importance of turgor changes in the HOG pathway activation/deactivation profile we employed a system in which yeast passively adapts to an osmotic shock. Parallel monitoring of different events in osmoadaptation confirms a scenario in which a drop in turgor first activates the HOG pathway and subsequent rapid accumulation of glycerol causes turgor increase resulting in signal cessation. The pathway is then deactivated by protein phosphatases.
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