The heat-shock response (HSR), the enhanced expression of one or more classes of molecular chaperones termed heat-shock proteins (Hsps) in response to stress induced by high temperatures, is commonly viewed as a "universal" characteristic of organisms. This project will examine the occurrence of the heat-shock response in a highly cold-adapted, stenothermal Antarctic teleost fish, Trematomus bernacchii, to determine whether this response has persisted in a lineage of fish that has encountered very low and stable temperatures for at least the past 14 - 25 million years. The principal investigator has demonstrated that the HSR has been lost in T. bernacchaa and the current proposal is designed to extend this initial and evolutionary significant observation. The proposed studies have two primary objectives. First, to establish how widespread the loss of the HSR might be in the suborder Notothenoioidei, including Antarctic and non-Antarctic members of the group. The second primary objective is to determine the nature of the lesion in gene expression that accounts for the loss of the expression of stress-inducible genes in Antarctic species. For both objectives, experiments will be conducted on closely related cold temperate species from New Zealand waters in order to gain phylogenetic and comparative insight into the nature of this profound change in enviro nmental regulation of gene expression. The results from this proposal will contribute to knowledge of the environmental physiology and evolutionary biology of the Antarctic notothenioid fishes and will extend an understanding of the extreme stenothermality in these fish. If evolution at subzero temperatures has indeed altered the gene expression patterns for molecular chaperones in Antarctic fish, this opens up an entire area of study into how cells respond to temperature at a molecular level. The heat shock response is the quintessential example of the environmental regulation of gene expression and, although the HSR is a well-described cellular phenomenon, there is not a great deal of information regarding how the response is regulated in ectothermic animals in nature. The lesions in the Hsp gene expression in Antarctic notothenioids may serve to highlight aspects of the "cellular thermostat" and provide key information about the mechanism by which environmental stress is transduced into a molecular response.
