Chill-Coma Tolerance, a Major Climatic Adaptation Among Drosophila Species

Gibert, Patricia; Moréteau, B.; Pétavy, Georges; Karan, Dev; David, Jean R.

doi:10.1554/0014-3820(2001)055[1063:cctamc]2.0.co;2

Cited by 204 publications

(120 citation statements)

References 23 publications

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“…, Castañeda et al 2005, Hoffmann et al 2005, Collinge et al 2006. Such variation in stress resistance might be associated with different thermal thresholds, allowing earlier activity in the morning, later activity in the evening and generally higher levels of activity under colder conditions (Gibert et al 2001, Watt et al 2003, Haag et al 2005.…”

Section: Temperature Stress Resistancementioning

confidence: 99%

Exploring plastic and genetic responses to temperature variation using copper butterflies

Fischer¹,

Karl²

2010

Clim. Res.

107

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Variable thermal environments experienced by most organisms warrant mechanisms to adjust the expression of phenotypic values to environmental needs. Here we explored short-(mainly developmental plasticity) and long-term effects (genetic differentiation across altitudes) of temperature variation using copper butterflies as model organisms. Lower compared to higher developmental temperatures yielded predictable variation by increasing development time, body size, total food consumption, the efficiency of converting digested food into body matter, and cold stress resistance, but decreasing daily food consumption, assimilation efficiency, body fat and protein content, weight loss at metamorphosis, the proportion of directly developing individuals, pupal melanisation and heat stress resistance. While variation in temperature stress resistance and developmental pathways is likely to reflect adaptive phenotypic plasticity, the reasons underlying variation in other traits are less clear. High-altitude populations showed increased development time, egg size, flight performance, wing and pupal melanisation and cold stress resistance, but decreased body fat content and heat stress resistance, compared to low-altitude populations. The differences seem to be mainly caused by thermal adaptation and seasonal time constraints. Cold stress resistance was related to variation at the phosphoglucose isomerase locus, and variation in heat stress resistance showed patterns similar to variation in the expression of stress-inducible heat shock proteins. High-altitude populations showed clearly reduced plasticity in heat stress tolerance, which may pose a substantial problem, given the rising temperatures at a global scale.

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Section: Temperature Stress Resistancementioning

confidence: 99%

Exploring plastic and genetic responses to temperature variation using copper butterflies

Fischer¹,

Karl²

2010

Clim. Res.

107

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“…Ayrinhac et al, 2004;Gaston and Chown, 1999;Gibert et al, 2001;Overgaard et al, 2014) and are generally regarded to be physiologically linked. In particular, CCRT is considered to require a reversal of the physiological state that induces chill coma (David et al, 1998;MacMillan and Sinclair, 2011a), and these two traits are generally considered equivalent measures of insect cold hardiness.…”

Section: Introductionmentioning

confidence: 99%

Cold-induced depolarization of insect muscle: Differing roles of extracellular K+ during acute and chronic chilling

MacMillan

Findsen

Pedersen

et al. 2014

Journal of Experimental Biology

111

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Insects enter chill coma, a reversible state of paralysis, at temperatures below their critical thermal minimum (CT min ), and the time required for an insect to recover after a cold exposure is termed chill coma recovery time (CCRT). The CT min and CCRT are both important metrics of insect cold tolerance that are used interchangeably, although chill coma recovery is not necessarily permitted by a direct reversal of the mechanism causing chill coma onset. Nevertheless, onset and recovery of coma have been attributed to loss of neuromuscular function due to depolarization of muscle fibre membrane potential (V m does depolarize muscle resting potential and slow CCRT following prolonged cold exposure. However, onset of chill coma at the CT min relates to an as-yet-unknown effect of temperature on neuromuscular function.

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“…However, if the cold exposure inducing chill coma is prolonged or severe the insects may accumulate chill injuries that ultimately result in death (Gibert et al, 2001;David et al, 2003;Koštál et al, 2004;Anderson et al, 2005;Koštál et al, 2006;MacMillan and Sinclair, 2011a). Chill sensitivity has been found in a wide range of insect orders including Coleoptera, Diptera, Hemiptera, Orthoptera and Hymenoptera (Lee et al, 1987a;Goller and Esch, 1990;Gibert et al, 2001;Koštál et al, 2004;Powell and Bale, 2004;Jing et al, 2005;Koštál et al, 2006;MacMillan and Sinclair, 2011a) and the chill coma temperature has been shown to be a powerful determinant of intraspecific variation in geographical distribution (Gibert et al, 2001;Kimura, 2004;Macdonald et al, 2004;Anderson et al, 2005;MacMillan and Sinclair, 2011b;Kellermann et al, 2012a). In spite of this, very little is known about the physiology of chill coma.…”

Section: Introductionmentioning

confidence: 99%

Rapid cold hardening improves recovery of ion homeostasis and chill coma recovery in the migratory locustLocusta migratoria

Findsen

Andersen

Calderon

et al. 2013

Journal of Experimental Biology

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Summary Chill tolerance of insects is defined as the ability of insects to tolerate low temperature under circumstances not involving freezing of intra- or extracellular fluids. For many insects chill tolerance is crucial for their ability to persist in cold environments and mounting evidence indicate that chill tolerance is associated with the ability to maintain ion- and water-homeostasis, thereby ensuring muscular function and preventing chill injury at low temperature. The present study describes the relationship between muscle and hemolymph ion-homeostasis and time to regain posture following cold shock (CS, 2h at -4°C) in the chill susceptible locust, Locusta migratoria. This relationship is examined in animals with and without a prior rapid cold hardening treatment (RCH, 2h at 0°C) to investigate the physiological underpinnings of RCH. Cold shock elicited a doubling of hemolymph [K+] and this disturbance was greater in locusts pre-exposed to RCH. Recovery of ion homeostasis was, however, markedly faster in RCH treated animals which correlated well with whole organism performance as hardened individuals regained posture more than 2 minutes faster than non-hardened individuals following CS. The present study indicates that loss and recovery of muscular function is associated with resting membrane potential of excitable membranes as attested from the changes in the equilibrium potential for K+ (EK) following CS. Both hardened and non-hardened animals recovered movement once K+ homeostasis was recovered to a fixed level (EK≈ -41 mV). RCH is therefore not associated with altered sensitivity to ion disturbance but instead a faster recovery of hemolymph [K+].

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Chill-Coma Tolerance, a Major Climatic Adaptation Among Drosophila Species

Cited by 204 publications

References 23 publications

Exploring plastic and genetic responses to temperature variation using copper butterflies

Exploring plastic and genetic responses to temperature variation using copper butterflies

Cold-induced depolarization of insect muscle: Differing roles of extracellular K+ during acute and chronic chilling

Rapid cold hardening improves recovery of ion homeostasis and chill coma recovery in the migratory locustLocusta migratoria

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