Abstract
The ability to quickly respond to changes in environmental temperature is critical for organisms living in thermally variable environments. To cope with sudden drops in temperature, insects and other ectotherms are capable of rapid cold hardening (RCH), in which mild chilling significantly enhances cold tolerance within minutes. While the ecological significance of RCH is well established, the mechanisms underlying RCH are still poorly understood. Previous work has demonstrated that RCH is regulated at the cellular level by post-translational signaling mechanisms, and here we tested the hypothesis that cultured cells are capable of RCH. A 2 h cold shock at -8°C significantly reduced the metabolic viability of Drosophila S2 cells, but pre-treatment with RCH at 4°C for 2 h prevented this decrease in viability. Thus, S2 cells are capable of RCH in a similar manner to whole insects and provide a new system for investigating the cell biology of RCH.
