Abstract
Insect cold tolerance depends on their ability to withstand or repair perturbations in cellular homeostasis caused by low temperature stress. Decreased oxygen availability (hypoxia) can interact with low temperature tolerance, often improving insect survival. One mechanism proposed for such responses is that whole-animal cold tolerance is set by a transition to anaerobic metabolism. Here, we provide a test of this hypothesis in an insect model system (Thaumatotibia leucotreta) by experimental manipulation of oxygen availability while measuring metabolic rate, critical thermal minimum (CTmin), supercooling point and changes in 43 metabolites in moth larvae at three key timepoints (before, during and after chill coma). Furthermore, we determined the critical oxygen partial pressure below which metabolic rate was suppressed (c. 4.5 kPa). Results showed that altering oxygen availability did not affect (non-lethal) CTmin nor (lethal) supercooling point. Metabolomic profiling revealed the upregulation of anaerobic metabolites and alterations in concentrations of citric acid cycle intermediates during and after chill coma exposure. Hypoxia exacerbated the anaerobic metabolite responses induced by low temperatures. These results suggest that cold tolerance of T. leucotreta larvae is not set by oxygen limitation, and that anaerobic metabolism in these larvae may contribute to their ability to survive in necrotic fruit.
Highlights
Which in turn may result in elevated respiratory water loss rates[18,19,20]
If chill coma endpoints are driven by oxygen availability, one major expectation is that hypoxia will increase critical thermal minima (CTmin) (=less cold tolerant) while hyperoxia would decrease CTmin (=more cold tolerant)13,15 – relative to normoxia
We show here that T. leucotreta larvae are likely not oxygen limited at low temperatures or during chill coma, as exposure to different PO2 levels does not influence their low temperature tolerance scored as either activity limits (CTmin) or lethal (SCP) limits
Summary
Increasing metabolic rate - or sustained opening of the spiracles at a given ambient oxygen concentration - may result in oxidative damage, assuming that cellular respiration rates remain constant These indirect changes can in turn affect CTmin and low temperature tolerance by influencing osmotic balance and, ion homeostasis and nerve transmission[10]. Previous research has shown the potential value of metabolomic profiling for investigating RCH or acclimation responses and cold shock Such studies have yielded insights into the dynamic changes associated with cold tolerance by providing correlations between temperature tolerance or rates of recovery from chilling, and specific metabolites and key biochemical energy pathways[28,29,30,31]. We predicted stronger anaerobic metabolite responses below, rather than above, Pcrit levels, with associated concomitant changes in low temperature tolerance more pronounced under conditions further from homeostasis setpoints
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