Heat shock

Basal thermotolerance

The temperature at which heat induces injury and/ or death varies both through space and in time. Because differences in methods of measurement usually assess different traits (e.g. knockdown resistance versus survival), resulting in dissimilar outcomes, it is difficult to reach general conclusions regarding upper thermotolerance limits. However, in insects they generally do not exceed about 53°C (Christian and Morton 1992), and are usually not much lower than 30°C, although these values depend on the trait being measured. There are examples of very low tolerance levels in some species such as alpine grylloblattids, and tolerance may increase dramatically in dormant, virtually anhydrobiotic, stages such as eggs. Ignoring these extreme values, substantial variation in tolerances remains. Geographic variation in thermotolerance levels, in the same direction as that of environmental temperature variation, is typical of both the species and population levels (Andrewartha and Birch 1954; Cloudsley-Thompson 1962; Stanley et al. 1980; Chen et al. 1990; Kimura et al. 1994; Goto et al. 2000), although variation among populations is sometimes less pronounced than that among species (Hercus et al. 2000).

However, the association between climatic conditions and tolerance is not always straightforward, especially because variation in thermotolerance often differs between developmental stages. For example, Krebs and Loeschcke (1995a) found that the rank order of resistance to high temperature stress in seven populations of Drosophila buzzatii differed among eggs, larvae, pupae, and adults. High resistance at one stage was not necessarily associated with high resistance at another. Likewise, Coyne et al. (1983) found that the nature of the variation in high temperature tolerance among populations of D. pseudoobscura depended on the stage being investigated. While there was significant interpopulation variation among adults and pupae, pupal variation was lower than that in the adults, and only pupal variation ranked in the same order as environmental variation. This variation is, perhaps, not surprising given that differences in the mobility of these stages are likely to mean differences in their exposure to extreme temperatures, and that the significance of different thermotolerance traits may change with development (see Section 5.1). However, this independence may not always be complete.

Investigations using both isofemale lines and selection in the laboratory have shown that there is considerable genetic variation in tolerance limits to high temperature, and that heritability of these traits is significant (Hoffmann and Parsons 1991). Laboratory selection, in particular, has demonstrated that developmental temperature has a marked effect on basal thermotolerance, such that improved resistance to high temperatures evolves both in populations evolving at higher temperatures (Cavicchi et al. 1995; Gilchrist et al. 1997), and those being selected for resistance to a high temperature treatment (Huey et al. 1992; Hoffmann et al. 1997) (Fig. 5.7). While the majority of studies have concerned Drosophila, several other species display similar responses to selection (e.g. Baldwin 1954; White et al. 1970). Because heat shock survival and knockdown temperature are genetically uncoupled (Section 5.1.2), knockdown generally does not respond to laboratory natural selection (Gilchrist et al. 1997), but does show a considerable response to artificial selection for knockdown resistance (Hoffmann et al. 1997). Although the pronounced response to selection in laboratory populations may be a consequence of loss of resistance following adaptation to laboratory conditions (Harshman and Hoffmann 2000; Hoffmann et al. 2001a), the combination of geographic variation of thermal tolerance under natural conditions, and responses to selection in the laboratory suggest that basal thermotolerance is a heritable trait that varies considerably between species and responds strongly to selection.

The physiological basis of this variation in ther-motolerance is much less clear. It has been suggested that constitutively expressed heat shock proteins (Hsps, see below) might be responsible for both survival of potentially lethal temperatures and for

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