Evidence for a rapid cold hardening response in cultured Drosophila S2 cells

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.

Identification of a neural basis for cold acclimation in Drosophila larvae

“…Of course, not all mechanisms of cold acclimation need be nervous system dependent. As previously mentioned, there is evidence that non-neuronal cells can detect cold via rapid calcium signaling, thereby driving nervous system independent cold hardening ( Nadeau and Teets, 2020 ; Teets et al., 2013 ).…”

“…A substantial and growing body of literature details how insect RCH and cold acclimation are mediated by a variety of physiological, genetic, and biochemical changes, many of which are tied to ionoregulatory balance ( Andersen and Overgaard, 2020 ; Bayley et al., 2020 ; Des Marteaux et al., 2018a , 2018b ; Gerber and Overgaard, 2018 ; MacMillan et al., 2016 ; Nadeau and Teets, 2020 ; Salehipour-shirazi et al., 2017 ; Toxopeus et al., 2019 ; Toxopeus and Sinclair, 2018 ). While there is evidence that aspects of RCH are mediated independently of the nervous system ( Nadeau and Teets, 2020 ; Teets et al., 2013 ), there is also evidence that absolute temperature information encoded by cold sensors drives changes in sleep and wakefulness, and that shutdown in the central nervous system (via spreading depolarization) is coincident with cold acclimation ( Alpert et al., 2020 ; Andersen et al., 2018 ). Yet, it remains unknown if the nervous system serves to proximally activate cold acclimation, or to what degree peripheral sensory neurons might function in this capacity—long-standing questions in the field of ectotherm biology ( Bowler, 2005 ; Lagerspetz, 1974 ; Prosser and Nelson, 1981 ).…”

Effects of a high cholesterol diet onDrosophilachill tolerance are highly context-dependent

“…While RCH can also improve cold tolerance, it is driven at least in part by mechanisms unrelated to those associated with cold acclimation (Teets and Denlinger, 2013). Unlike acclimation, RCH is thought to occur mostly at the cellular level, having been demonstrated in isolated cells in vitro (Nadeau and Teets, 2020; Yi and Lee, 2004).…”

The evolution of cold nociception in drosophilid larvae and identification of a neural basis for cold acclimation

“…A substantial and growing body of literature details how insect RCH and cold acclimation are mediated by a variety of physiological, genetic, and biochemical changes, many of which are tied to ionoregulatory balance (8)(9)(10)(11)(12)(13)(14)(15)(16)(17). There is also evidence that absolute temperature information encoded by cold sensors drives changes in sleep and wakefulness, and that shutdown in the central nervous system (via spreading depolarization) is coincident with cold acclimation (18,19).…”