Survival under stress: molecular mechanisms of metabolic rate depression in animals
Kenneth B. Storey
For many species, survival under harsh environmental conditions includes metabolic rate depression, an escape into a hypometabolic or dormant state. Studies in my laboratory are analysing the molecular mechanisms and regulatory events that underlie transitions to and from hypometabolic states In systems including anoxia-tolerant turtles and molluscs, estivating snails and toads, hibernating small mammals, and freeze tolerant frogs and insects. Our newest research targets two areas: the role of protein kinases in regulating metabolic adjustments and the role of stress-induced gene expression in producing specific adaptive proteins. Protein kinases A, C and G are all linked to stress-induced signal transduction in various systems, and new studies also show tissue-specific activation of mitogen-activated protein kinases (ERK, JNK, see list of abbreviations p38). Protein adaptations supporting stress tolerance are being sought using cDNA library screening, differential display PCR and Northern blotting to analyse gene expression. These techniques offer new insights into the types of cellular targets that must be coordinated to achieve metabolic suppression and facilitate easy analysis of organ-, time-, and stress-specific gene expression. For example, freeze-induced gene expression in frog liver includes upregulation of genes for subunits of fibrinogen and ADP/ATP translocase, whereas mitochondrial genes coding for subunits of NADH-ubiquinone oxidoreductase subunit 5 and cytochrome C oxidase subunit 1 were upregulated during anoxia in turtle heart.