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Osmotolerance and osmoadaption

Osmoregulation in yeast is dependent on the capacity to sense external stimuli and the resultant changes in physiology, biochemistry, and other cellular functions to meet the modified needs of the cell in light of that environmental change. There are two forms of ‘response' that any cell may apply following exposure to osmotic challenge: osmotol- erance and osmoadaption.

Osmotolerance is strain-dependent and refers to the capacity of a strain to withstand osmotic imbalances (Werner-Washburne et al., 1993; Hounsa et al., 1998; Gasch and Werner-Washburne, 2002). In this scenario, tolerance is derived from an innate ability to withstand the deleterious effects of hyperosmotic pressure as a consequence of ‘superior' membrane structure, vacuolar functioning, residual trehalose levels, and many other intrinsic factors (Latterich and Watson, 1991; Sharma et al., 1996; Singer and Lindquist, 1998; Nass and Rao, 1999). Indeed, osmotolerance is promoted by the abundance of osmoprotectant macromolecules that stabilize cellular membranes, enzymes, other proteins, and possibly nucleic acids, with little effect on the intracellular water potential (Hernandez- Saavedra et al., 1995).

Osmoadaption typically involves the cessation of replication (Poolman and Glaasker 1998) in favour of survival mode. The process involves a highly refined sensing and response system that is activated in either acute or chronic form. Nass and Rao (1999) defined the chronic response (or acquired osmotolerance) as a signal transduction-mediated pathway that alters the levels of specific proteins, whereas the acute response is a rapid response invoked in response to sudden shifts in high external osmolarity. Both involve the accumulation of one or more types of molecule, termed osmoticum (pl = osmotica), within the cell in order to increase intracellular osmotic potential, and thus prevent cellular water loss (Yancey et al., 1982; Wegmann, 1986; Blomberg and Adler, 1992; Hernandez- Saavedra et al., 1995). One subclass of osmotica, the compatible solutes, have very little effect on normal cellular functioning when accumulated at high levels (Poolman and Glaasker 1998) but the accumulation of this solute causes the cell to retain water that would otherwise be effluxed. Their role in stabilizing the cell during hyperosmotic stress is therefore crucial.

Glycerol is the key compatible solute accumulated during osmotic stress (Brown, 1978; Brown et al., 1986, Blomberg and Adler, 1989, 1992, Albertyn et al., 1994; Hohmann, 1997), and deletions in key genes encoding enzymes in the glycerol biosynthetic pathway lead to an inability to survive hyperosmotic conditions (Albertyn et al., 1994; Eriksson et al., 1995; Liden et al., 1996; Ansell et al., 1997; Hounsa et al., 1998). Glycerol has an important secondary role to play in anaerobic stress, as the requirement of NAD+ in its production enables glycerol to serve as the final product in a ‘redox dump' pathway (Ansell et al., 1997) and this is also relevant to brewing yeast fermentations. Cells subjected to high external osmolarity are able to effectively sense this external stimulus using two surface sensor proteins, Sln1p and Sho1p (Maeda et al., 1994, 1995), which results in the activation of the HOG (MAP kinase) pathway. The HOG stimulates the hyperproduction and hyperaccumulation of glycerol as a compatible solute in order to balance the external and internal osmolarities (Albertyn et al., 1994; Remize et al., 2001; Pahl- man et al., 2001). It also appears to mediate the activity of the glyceroaquaporin Fps1p (Luyten et al., 1994; Tamas et al., 1999), which reduces the net efflux of glycerol and thus aids intracellular accumulation.

Saccharomyces spp. and other yeasts show a change in cell size concurrent with external osmo- larity changes (Hohmann, 1997). An increase in external osmolarity results in a rapid loss of intracellular water and thus cell shrinkage (Morris et al., 1986; Blomberg and Adler, 1992; Hohmann, 1997). Restoration of favourable (isotonic) solute conditions to hyperosmotically stressed cells does not, however, result in cells regaining their former volume (Hohmann, 1997).

 
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