The general stress response
Saccharomyces cerevisiae demonstrates two major stress response pathways, the heat shock response (HSR), which is activated in a complex manner by sublethal heat stress (Chatterjee et al., 2000) and mediated by the so-called heat shock transcription factor (HSF) (Bienz and Pelham, 1986; Morimoto et al., 1996). Alternatively, the general (or global) stress response (GSR) is activated by a number of environmental stresses including oxidative, pH, heat, and osmotic stresses, as well as nitrogen starvation (Ruis and Schuller, 1995; Schmitt and McEntee, 1996; Martinez-Pastor et al., 1996). The GSR is believed to be an evolutionary adaptation that allows yeast to respond to adverse environmental conditions in a non-specific manner, in order that cellular fecundity is retained whilst specific responses are activated (Ruis and Schuller, 1995; Martinez-Pastor et al., 1996). The GSR is typified by the up-regulation of approximately 200 genes and their corresponding proteins, which are involved in a diverse array of cellular functions (Gasch et al., 2000; Causton et al., 2001). The expression of these genes has been demonstrated to occur in a process dependent upon the pentameric cis-acting sequence CCCCT within the promoter region of the induced genes. This so-called stress responsive element (STRE) was first identified in reference to the stress-induced expression of the CTT1 gene encoding cytosolic catalase T (Marchler et al., 1993) and subsequently in control of expression of the DDR2 gene, which encodes a putative chaperone protein (Kobayashi and McEntee, 1993). It has subsequently been demonstrated that the activation of the STRE element of inducible genes is dependent upon two zinc finger transcriptional activators (Msn2p and Msn4p) (Martinez-Pastor et al., 1996; Schmitt and McEntee, 1996; Treger et al., 1998), which are active during a wide array of stresses (Ruis and Schuller, 1995; Hohmann,
2002), including those associated with yeast handling in the industrial brewery and during the diauxic shift (Boy-Marcotte et al., 1998). This mode of activation explains why exposure to one type of stress often confers resistance to another, unrelated form of stress (Lindquist, 1986). The general stress response is a transient phenomenon and Msn2p is rapidly degraded following the stress response (Bose et al., 2005).