Temperature-Induced Hormesis in Drosophila

Abstract

The phenomenon that a mild exposure to an otherwise detrimental stress factor can be beneficial, termed hormesis, is well known for many organisms and life-history traits (Khazaeli et al. 1997; Le Bourg and Minois 1997; Bubliy et al. 1998; Minois 2000; Parsons 2000). Mild stress treatments have been shown to induce hormesis in mammals and insects (Rattan 1998; Minois 2000; Le Bourg et al. 2001; Hercus et al. 2003) and increased performance has been reported with respect to, e.g., delayed aging, increased longevity and (heat) resistance to severe stress long after the hormesis inducing stress was applied (Le Bourg and Minois 1999; Hercus et al. 2003, as exemplified in Fig. 1). Thus, mild stress exposure may have long-lasting effects, much longer than the vast majority of the stress-induced changes in metabolites, proteins and gene expression (Dahlgaard et al. 1998; Sorensen et al. 2005; Malmendal et al. 2006). High temperature is one of the stress factors that has been shown to induce hormesis (Rattan 1998; Le Bourg et al. 2001; Hercus et al. 2003; Kristensen et al. 2003; Scannapieco et al. 2007). The reason for choosing high temperature as a model stress is that it is easy to expose experimental organisms to well-defined thermal regimes and because it is a natural occurring stress for many plant and animal species that often are not able to avoid high temperatures in their environment. Thus, it can be expected that adaptations to temperature/heat stress are frequent in nature. Furthermore heat stress shares characteristics with other stress factors, e.g., the type of cellular damage induced, and induces a suit of relatively well-studied molecular chaperones through the heat shock response, which are among the prime candidates conferring hormetic effects. Effects of exposure to stressful low temperatures show similarities to exposure to high temperatures as both induce cellular