SUMMARYDuring cold periods ectotherms may improve low temperature tolerance via rapid cold hardening (RCH) over a period of hours and/or long-term cold acclimation (LTCA) during days, weeks or months. However, the effect of duration and the major underlying mechanisms of these processes are still not fully understood. In the present study, the molecular and biochemical responses to RCH (1-3h) and LTCA (1-3days) and the corresponding benefits to survival were investigated using the chill-sensitive collembolan Folsomia candida. We investigated osmolyte accumulation, membrane restructuring and transcription of candidate genes as well as survival benefits in response to RCH and LTCA. RCH induced significant upregulation of targeted genes encoding enzymes related to carbohydrate metabolic pathways and genes encoding small and constitutively expressed heat shock proteins (Hsps), indicating that the animals rely on protein protection from a subset of Hsps during RCH and probably also LTCA. The upregulation of genes involved in carbohydrate metabolic processes initiated during RCH was likely responsible for a transient accumulation of myoinositol during LTCA, which may support the protection of protein and membrane function and structure. Membrane restructuring, composed especially of a significantly increased ratio of unsaturated to saturated phospholipid fatty acids seems to be a mechanism supplementary to activation of Hsps and myoinositol accumulation in LTCA. Thus, the moderate increase in cold shock tolerance conferred by RCH seems to be dominated by effects of Hsps, whereas the substantially better cold tolerance achieved after LTCA is dominated by post-transcriptional processes increasing membrane fluidity and cryoprotectant concentration.

Contaminants taken up by living organisms in the environment as a result of anthropogenic contamination can reduce the tolerance of natural stressors, e.g., low temperatures, but the physiological mechanisms behind these interactions of effects are poorly understood. The tolerance to low temperatures of organisms that cannot regulate their body temperature (ectotherms) depends on their ability to increase the fluidity of their cellular membranes at low temperatures. Our study shows that contaminants accumulating in lipids of organisms alter the physical state of their membranes simply by being present. Contaminants of varying chemical structures can alter the membrane fluidity in either direction and correspondingly modulate the cold tolerance of intact animals.

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