Biology subjects

Jorgensen, L. B.

Publications and source records attributed to Jorgensen, L. B..

3 recordsLinked to original sources

bioRxiv2022

Balanced mitochondrial function at low temperature is linked to cold adaptation in Drosophila species

The ability of ectothermic animals to live in different thermal environments is closely associated with their capacity to maintain physiological homeostasis across diurnal and seasonal temperature fluctuations. For chill-susceptible insects, such as Drosophila, cold tolerance is tightly linked to ion and water homeostasis obtained through a regulated balance of active and passive transport. Active transport at low temperature requires a constant delivery of ATP and we therefore hypothesize that cold-adapted Drosophila are characterized by superior mitochondrial capacity at low temperature relative cold-sensitive species. To address this, we investigated how experimental temperatures 19-1 {degrees}C affected mitochondrial substrate oxidation in flight muscle of seven tropical and temperate Drosophila species that represent a broad spectrum of cold tolerance. Mitochondrial oxygen consumption rates measured using a substrate-uncoupler-inhibitor-titration protocol showed that cooling generally reduced oxygen consumption of all steps of the electron transport system across species. Complex I is the primary consumer of oxygen at benign temperatures, but low temperature decreases complex I respiration to a much greater extent in cold-sensitive species than in cold-adapted species. Accordingly, cold-induced reduction of complex I correlates strongly with CTmin (the temperature inducing cold coma). The relative contribution of alternative substrates, proline, succinate and glycerol-3-phosphate increased as temperature decreased, particularly in the cold-sensitive species. At present it is unclear whether the oxidation of alternative substrates can be used to offset the effects of the temperature-sensitive complex I, and the potential functional consequences of such a substrate switch are discussed. Summary statementMitochondrial oxygen consumption decreases at low temperature, particularly in cold-sensitive Drosophila species, which turn to oxidation of alternative substrates as complex I-supported respiration is impaired.

physiology↗

bioRxiv2020

Dramatic changes in mitochondrial substrate use at critically high temperatures: a comparative study using Drosophila

Ectotherm thermal tolerance is critical to species distribution, but at present the physiological underpinnings of heat tolerance remain poorly understood. Mitochondrial function is perturbed at critically high temperatures in some ectotherms, including insects, suggesting that heat tolerance of these animals is linked to failure of oxidative phosphorylation (OXPHOS) and/or ATP production. To test this hypothesis we measured mitochondrial oxygen consumption rates in six Drosophila species with different heat tolerance using high-resolution respirometry. Using a substrate-uncoupler-inhibitor titration protocol we examined specific steps of the electron transport system to study how temperatures below, bracketing and above organismal heat limits affected mitochondrial function and substrate oxidation. At benign temperatures (19 and 30{degrees}C), complex I-supported respiration (CI-OXPHOS) was the most significant contributor to maximal OXPHOS. At higher temperatures (34, 38, 42 and 46{degrees}C), CI-OXPHOS decreased considerably, ultimately to very low levels at 42 and 46{degrees}C. The enzymatic catalytic capacity of complex I was intact across all temperatures and accordingly the decreased CI-OXPHOS is unlikely to be caused directly by hyperthermic denaturation/inactivation of complex I. Despite the reduction in CI-OXPHOS, maximal OXPHOS capacities were maintained in all species, through oxidation of alternative substrates; proline, succinate and, particularly, glycerol-3-phosphate, suggesting important mitochondrial flexibility at temperatures exceeding the organismal heat limit. Interestingly, this compensatory oxidation of alternative substrates occurred at temperatures that tended to correlate with species heat tolerance, such that heat-tolerant species could defend "normal" mitochondrial function at higher temperatures than sensitive species. Future studies should investigate why CI-OXPHOS is perturbed and how this potentially affects ATP production rates.

physiology↗

bioRxiv2019

Neural dysfunction correlates with heat coma and CTmax in Drosophila but does not set the boundaries for heat stress survival

When heated, insects loose coordinated movement followed by the onset of heat coma (CTmax). These phenotypes are popular measures to quantify inter- and intraspecific differences in insect heat tolerance, and CTmax correlate well with current species distributions. Here we examined the function of the central nervous system (CNS) in five species of Drosophila with different heat tolerances, while they were exposed to either constant high temperature or a gradual increasing temperature (ramp). Tolerant species were able to preserve CNS function at higher temperatures and for longer durations than sensitive species and similar differences were found for the behavioral indices (loss of coordination and onset of heat coma). Furthermore, the timing and temperature (constant and ramp exposure, respectively) for loss of coordination or complete coma coincided with the occurrence of spreading depolarisation (SD) events in the CNS. These SD events disrupt neurological function and silence the CNS suggesting that CNS failure is the primary cause of impaired coordination and heat coma. Heat mortality occurs soon after heat coma in insects and to examine if CNS failure could also be the proximal cause of heat death, we used selective heating of the head (CNS) and abdomen (visceral tissues). When comparing the temperature causing 50% mortality (LT50) of each body part to that of the whole animal, we found that the head was not particularly heat sensitive compared to the abdomen. Accordingly, it is unlikely that nervous failure is the principal/proximate cause of heat mortality in Drosophila. Summary statementHyperthermic failure of the Drosophila central nervous system causes heat coma, a phenotype varying in temperature between drosophilids, but neural failure is likely not the primary cause of heat mortality.

physiology↗