A Rapid Cold-Hardening Process in Insects

Lee, Richard; Chen, Cheng‐Ping; Denlinger, David L.

doi:10.1126/science.238.4832.1415

Cited by 423 publications

(310 citation statements)

References 8 publications

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“…Although RCH has been described in many species, the mechanisms are not well understood (Chown and Nicholson, 2004). Lee et al (1987) found an increase in concentration of the common carbohydrate cryoprotectant glycerol after 0 °C pre-treatments in the flesh fly (Sarcophaga crassipalpis) to 81.3 mM, nearly three times the levels found in prechilled organisms. Although the changes were not large enough to have a colligative effect (i.e.…”

Section: Introductionmentioning

confidence: 87%

“…A number of insects that suffer from non-freezing cold injury are nevertheless able to rapidly alter their tolerance of acute cold exposure by rapid cold-hardening (RCH; Lee et al, 1987), whereby low temperature tolerance is greatly enhanced by a short pre-exposure to a milder low temperature. For example, Czajka and Lee (1990) showed that adult Drosophila melanogaster will die (but not freeze) when exposed to −5 °C for 2 h, but if chilled at 5 °C for as little as 2 h prior to the subzero treatment, most will survive.…”

Section: Introductionmentioning

confidence: 99%

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The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

Nilson

Sinclair

Roberts

2006

Journal of Insect Physiology

120

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Carbon dioxide gas is used as an insect anesthetic in many laboratories, despite recent studies which have shown that CO 2 can alter behavior and fitness. We examine the effects of CO 2 and anoxia (N 2 ) on cold tolerance, measuring the rapid cold-hardening (RCH) response and chill coma recovery in Drosophila melanogaster. Short exposures to CO 2 or N 2 do not significantly affect RCH, but 60 min of exposure negates RCH. Exposure to CO 2 anesthesia increases chill coma recovery time, but this effect disappears if the flies are given 90 min recovery in air before chill coma induction. Flies treated with N 2 show a similar pattern, but require significantly longer chill coma recovery times even after 90 min of recovery from anoxia. Our results suggest that CO 2 anesthesia is an acceptable way to manipulate flies before cold tolerance experiments (when using RCH or chill coma recovery as a measure), provided exposure duration is minimized and recovery is permitted before chill coma induction. However, we recommend that exposure to N 2 not be used as a method of anesthesia for chill coma studies.

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Section: Introductionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

Nilson

Sinclair

Roberts

2006

Journal of Insect Physiology

120

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“…Specifically, we measured whether capa knockdown impacts acute cold shock tolerance, the capacity for rapid cold hardening (RCH), and chill coma recovery time (CCR). RCH is an extreme case of rapid acclimation whereby brief (minutes to hours) nonlethal chilling significantly enhances cold-shock tolerance (35). CCR is a commonly used assay to assess the time required to regain coordinated movement after nonlethal chilling injury and frequently is used as an indicator of cold tolerance, especially in Drosophila species (16,36).…”

Section: Capa Neuropeptides Are Released Not During Desiccation and Coldmentioning

confidence: 99%

Insect capa neuropeptides impact desiccation and cold tolerance

Terhzaz

Teets

Cabrero

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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107

128

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The success of insects is linked to their impressive tolerance to environmental stress, but little is known about how such responses are mediated by the neuroendocrine system. Here we show that the capability (capa) neuropeptide gene is a desiccation-and cold stressresponsive gene in diverse dipteran species. Using targeted in vivo gene silencing, physiological manipulations, stress-tolerance assays, and rationally designed neuropeptide analogs, we demonstrate that the Drosophila melanogaster capa neuropeptide gene and its encoded peptides alter desiccation and cold tolerance. Knockdown of the capa gene increases desiccation tolerance but lengthens chill coma recovery time, and injection of capa peptide analogs can reverse both phenotypes. Immunohistochemical staining suggests that capa accumulates in the capa-expressing Va neurons during desiccation and nonlethal cold stress but is not released until recovery from each stress. Our results also suggest that regulation of cellular ion and water homeostasis mediated by capa peptide signaling in the insect Malpighian (renal) tubules is a key physiological mechanism during recovery from desiccation and cold stress. This work augments our understanding of how stress tolerance is mediated by neuroendocrine signaling and illustrates the use of rationally designed peptide analogs as agents for disrupting protective stress tolerance.environmental stress | insects | neuropeptides | capa | desiccation and cold tolerance

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“…Physiological studies in various organisms show that mild stress can increase the hardiness of the organism to the same but harsher stress (Bowler, 2005). Rapid Cold Hardening (RCH), an increase in cold tolerance after a prior (sub-lethal) exposure to cold, first described by Lee et al (1987) has been observed in numerous insect groups (Meats, 1973;Chown and Terblanche, 2007) including isolated tissue and cells (Yi and Lee, 2003).…”

Section: Introductionmentioning

confidence: 99%

Short-term hardening effects on survival of acute and chronic cold exposure by Drosophila melanogaster larvae

Rajamohan

Sinclair

2008

Journal of Insect Physiology

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We quantified the variation and plasticity in cold tolerance among four larval stages of four laboratory strains of Drosophila melanogaster in response to both acute (<2 hours of cold exposure) and chronic (∼7 hours of cold exposure) cold exposure. We observed significant differences in basal cold tolerance between the strains and among larval stages. Early larval instars were generally more tolerant of acute cold exposures than 3 rd instar larvae. However, wandering larvae were more tolerant of chronic cold exposures than the other stages. Early stages also displayed a more pronounced rapid cold-hardening response than the later stages. Heat pre-treatment did not confer a significant increase in cold tolerance to any of the strains at any stage, pointing to different mechanisms being involved in resolving heat-and cold-elicited damage. However, when heat pre-treatment was combined with rapid cold-hardening as sequential pre-treatments, both positive (heat first) and negative (heat second) effects on cold tolerance were observed. We discuss possible mechanisms underlying coldhardening and the effects of acute and chronic cold exposures.

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A Rapid Cold-Hardening Process in Insects

Cited by 423 publications

References 8 publications

The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

Insect capa neuropeptides impact desiccation and cold tolerance

Short-term hardening effects on survival of acute and chronic cold exposure by Drosophila melanogaster larvae

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