EXTENDED ABSTRACT ONLY – DO NOT CITE

The focus of stress research in fish has recently grown to encompass the cellular stress response in addition to that of the whole animal, broadening our understanding of the mechanisms allowing an animal to tolerate stress. Much of this expanded interest has focused on heat shock proteins and their role as molecular chaperones in the cellular response to stress (Iwama et al, 1998; Feder and Hofmann, 1999). Although HSPs have a relatively short half-life, their levels remain elevated in the whole organisms long after the stressor is removed, indicating a role in long term adaptation and increased stress tolerance (Parsell and Lindquist 1993; Morimoto and Santoro 1998). By artificially enhancing a fish’s stress tolerance both in vivo and in vitro, through exposure to a mild heat shock, we have been able to explore some of the pathways involved in the protection against stress in fish hepatocytes, and to relate these to the physiological changes that occur in the whole animal. This phenomenon of cross protection, or the ability of a mild stressor to transiently increase the tolerance of an animal to a subsequent heterologous stressor, has not been well documented in fish. We have begun to define and describe cross protection in fish in vivo and more recently have used cross protection as a model to identify some of the critical pathways regulating the cellular stress response in fish in vitro