Induced cold-tolerance mechanisms depend on duration of acclimation in the chillsensitive Folsomia candida (Collembola)

Summary During 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 hours) 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 up-regulation of targeted genes encoding enzymes related to carbohydrate metabolic pathways and genes encoding small and constitutively expressed Hsps, indicating that the animals rely on protein protection from a subset of Hsps during RCH and probably also LTCA. The up-regulation 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 supplementary mechanism 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 heat shock proteins, whereas the substantially better cold tolerance achieved after LTCA is dominated by post-transcriptional processes increasing membrane fluidity and cryoprotectant concentration.