Protection of poikilothermic animals from seasonal cold is widely regarded as being causally linked to changes in the unsaturation of membrane phospholipids, yet in animals this proposition remains formally untested. We have now achieved this by the genetic manipulation of lipid biosynthesis of Caenorhabditis elegans independent of temperature. Worms transferred from 25 degrees C to 10 degrees C develop over several days a much-increased tolerance of lethal cold (0 degrees C) and also an increased phospholipid unsaturation, as in higher animal models. Of the three C. elegans Delta9-desaturases, transcript levels of fat-7 only were up-regulated by cold transfer. RNAi suppression of fat-7 caused the induction of fat-5 desaturase, so to control desaturase expression we combined RNAi of fat-7 with a fat-5 knockout. These fat-5/fat-7 manipulated worms displayed the expected negative linear relationship between lipid saturation and cold tolerance at 0 degrees C, an outcome confirmed by dietary rescue. However, this change in lipid saturation explains just 16% of the observed difference between cold tolerance of animals held at 25 degrees C and 10 degrees C. Thus, although the manipulated lipid saturation affects the tolerable thermal window, and altered Delta9-desaturase expression accounts for cold-induced lipid adjustments, the effect is relatively small and none of the lipid manipulations were sufficient to convert worms between fully cold-sensitive and fully cold-tolerant states. Critically, transfer of 10 degrees C-acclimated worms back to 25 degrees C led to them restoring the usual cold-sensitive phenotype within 24 h despite retaining a lipid profile characteristic of 10 degrees C worms. Other nonlipid mechanisms of acquired cold protection clearly dominate inducible cold tolerance.
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