(or hardening), as many of the studies have done to date (Krebs and Bettencourt 1999).

Induced tolerance or hardening

It has long been appreciated that injury caused by high temperature can be ameliorated by prior exposure to a sublethal, or moderately high temperature (Hutchison and Maness 1979; Denlinger et al. 1991; Hoffmann and Watson 1993). This acclimation response lasts for several hours, but is nonetheless transient (Krebs and Loeschcke 1995b). Like basal tolerance, induced thermotolerance responds strongly both to artificial selection (Krebs and Loeschcke 1996), and to laboratory natural selection (Cavicchi et al. 1995), and it is clear that this trait shows considerable genetic variation (Loeschcke et al. 1994,1997; Krebs and Loeschcke 1997). However, variation between populations is not always apparent (Hoffmann and Watson 1993; Krebs and Loeschcke 1995a,b), although this depends to some extent on the temperature of the heat shock. Likewise, induced thermotolerance differs substantially between life stages in some cases, but not in others (Krebs and Loeschcke 1995a,b).

Interspecific differences in induced tolerance also appear counterintuitive in the sense that species from warmer environments often have a reduced response to hardening compared to those from more temperate climates (Chen et al. 1990). A reduced response to high temperature acclimation has also been found in populations of D. buzzatii, with a population from a low altitude, warm environment, showing little or no response to acclimation compared with one from a cool, high-altitude area (Sorensen et al. 2001). Similar results have also been found in laboratory selection experiments. For example, Cavicchi et al. (1995) showed that a line of D. melanogaster reared at 28°C lost its capacity for induced thermotolerance compared with lines reared at lower temperatures, and this finding was substantiated by Bettencourt et al. (1999). This reduced hardening response is probably a consequence of the costs of acclimation, which largely entail a reduction in development rate, fecundity, and survival (Krebs and Loeschcke 1994; Hoffmann 1995; Krebs et al. 1998). At least in the case of heat shock, this cost appears to be associated with the expression of heat shock proteins.

Heat shock proteins: benefits and costs Several studies of genetically engineered D. melanogaster have demonstrated both the costs and benefits of Hsp70 expression. The first set of studies involved two strains of D. melanogaster produced by Welte et al. (1993). One of the strains (excision) possesses the usual 10 copies of the hsp70 gene, while the second strain (extra-copy) has an additional 12 transgenic copies. The strains differ in no other ways, and the possible effects of mutagen-esis, that can make comparative work problematic, are largely controlled for, because of the way in which the strains were engineered (Feder and Krebs 1998).

After a 36°C pretreatment, the extra-copy strain shows both improved survival of 39°C and an increase in Hsp70 relative to the excision strain (Fig. 5.9) (Feder et al. 1996). This difference is particularly pronounced at pretreatment (hardening) temperatures that are either relatively low or relatively short in duration (Krebs and Feder 1998a). Once a reasonably high hardening temperature is reached (36°C) and the treatment is prolonged, the two strains show similar levels of Hsp70 expression. Thus, after the stage at which the capacity to express Hsp70 reaches full development, hsp70 copy number no longer enhances inducible ther-motolerance, despite differences in Hsp70 levels (Feder 1999; Tatar 1999). Nonetheless, it is clear that the possession of extra copies of hsp70, and consequently a higher level of Hsp70, enhances heat shock tolerance.

Further examination of the sites at which Hsp70 is important in providing protection against heat shock has revealed that the gut is especially sensitive to high temperature (Feder and Krebs 1998; Krebs and Feder 1998a). By using a second genetically engineered D. melanogaster mutant, mths70a, which causes the gut to express Hsp70 when reared on medium that contains 2 mM copper, Feder and Krebs (1998) showed that in the absence of hardening the mutant has considerably greater ingestion rates when reared on copper than when the metal is absent. However, with hardening and without heat shock, uptake rates are the same in both treatments (with and without copper). This provides clear evidence that Hsp70 has a considerable role in protecting the gut against heat shock. Using

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