In insects and other ectotherms,cold temperatures cause a coma resulting from loss of neuromuscular function,during which ionic and metabolic homeostasis are progressively lost.Cold adaptation improves homeostasis dur...In insects and other ectotherms,cold temperatures cause a coma resulting from loss of neuromuscular function,during which ionic and metabolic homeostasis are progressively lost.Cold adaptation improves homeostasis during cold exposure,but the ultimate targets of selection are still an open question.Cold acclimation and adaptation remodels mitochondrial metabolism in insects,suggesting that aerobic energy production during cold exposure could be a target of selection.Here,we test the hypothesis that cold adaptation improves the ability to maintain rates of aerobic energy production during cold exposure by using^(31)P NMR on live flies.Using lines of Drosophila melanogaster artificially selected for fast and slow recovery from a cold coma,we show that cold exposure does not lower ATP levels and that cold adaptation does not alter aerobic ATP production during cold exposure.Cold-hardy and cold-susceptible lines both experienced a brief transition to anaerobic metabolism during cooling,but this was rapidly reversed during cold exposure,suggesting that oxidative phosphorylation was sufficient to meet energy demands below the critical thermal minimum,even in cold-susceptible flies.We thus reject the hypothesis that performance under mild low temperatures is set by aerobic ATP supply limitations in D.melanogaster,excluding oxygen and capacity limitation as a weak link in energy supply.This work suggests that the modulations to mitochondrial metabolism resulting from cold acclimation or adaptation may arise from selection on a biosynthetic product(s)of those pathways rather than selection on ATP supply during cold exposure.展开更多
基金This work was performed in the McKnight Brain Institute at the National High Magnetic Field Laboratory’s AMRIS Facility,which is supported by National Science Foundation Cooperative Agreement No.DMR-1157490 and the State of FloridaThis work was supported in part by an NIH award,S10RR031637,for magnetic resonance instrumentation,and by National Science Foundation(NSF)Grants IOS-1051770(to T.J.M.)+3 种基金IOS-1051890(to D.A.H,A.S.E and D.B.A.)and IOS-1558159 to CMW.A.S.Ereceived partial support from the Georgia Research Alliance,and D.A.H.received support from the IAEA/FAO CRP on Dormancy management to enable mass rearing and increase efficacy of sterile insects and natural enemiesDan Plant provided valuable assistance setting up NMR experiments in AMRIS.Stephanie Dickinson checked the statistical analysesD.B.A was supported by NIH grants U24AG056053 and P30AG050886.
文摘In insects and other ectotherms,cold temperatures cause a coma resulting from loss of neuromuscular function,during which ionic and metabolic homeostasis are progressively lost.Cold adaptation improves homeostasis during cold exposure,but the ultimate targets of selection are still an open question.Cold acclimation and adaptation remodels mitochondrial metabolism in insects,suggesting that aerobic energy production during cold exposure could be a target of selection.Here,we test the hypothesis that cold adaptation improves the ability to maintain rates of aerobic energy production during cold exposure by using^(31)P NMR on live flies.Using lines of Drosophila melanogaster artificially selected for fast and slow recovery from a cold coma,we show that cold exposure does not lower ATP levels and that cold adaptation does not alter aerobic ATP production during cold exposure.Cold-hardy and cold-susceptible lines both experienced a brief transition to anaerobic metabolism during cooling,but this was rapidly reversed during cold exposure,suggesting that oxidative phosphorylation was sufficient to meet energy demands below the critical thermal minimum,even in cold-susceptible flies.We thus reject the hypothesis that performance under mild low temperatures is set by aerobic ATP supply limitations in D.melanogaster,excluding oxygen and capacity limitation as a weak link in energy supply.This work suggests that the modulations to mitochondrial metabolism resulting from cold acclimation or adaptation may arise from selection on a biosynthetic product(s)of those pathways rather than selection on ATP supply during cold exposure.
