Biology subjects

Willot, Q.

Publications and source records attributed to Willot, Q..

4 recordsLinked to original sources

bioRxiv2023

Cold Comfort: metabolic rate and tolerance to low temperatures predict latitudinal distribution in ants

Metabolic compensation has been proposed as a mean for ectotherms to cope with colder climates. For example, under the metabolic cold adaptation/metabolic homeostasis hypotheses (MCA/MHH), it has been formulated that cold-adapted ectotherms should display higher/more thermally sensitive metabolic rates (MRs) at lower temperatures. However, whether such compensation can truly be associated with distribution, and whether it interplays with cold-tolerance to support species climatic niches, remains largely unclear despite broad ecological implications thereof. Here, we teased apart the relationship between MRs, cold-tolerance, and distribution, to confront the MCA/MHH among 13 ant species. We report clear metabolic compensation effects, consistent with the MCA and MHH, where MR parameters strongly correlated with latitude and climatic factors across species distributions. The combination of both cold-tolerance and MR further upheld the best predictions of species climatic niches. To our knowledge, this is the first study showing that the association of metabolic data with cold-tolerance supports increased predictive value for biogeographical models in social insects. These results also highlight that adaptation to higher latitudes in ants involved adjustments of both cold-tolerance and MRs, potentially at the expense of metabolic performance at warmer temperatures, to allow this extremely successful group of insects to thrive under colder climates.

evolutionary biology↗

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↗

bioRxiv2022

Facing lethal temperatures: heat shock response in desert and temperate ants

Several genera of desert ants have adapted to endure prolonged exposure to high temperatures. The study of these ants is essential to unravel how species respond and adapt to thermal stress. We investigated the thermal tolerance and the transcriptomic heat stress response of three desert ant genera (Cataglyphis, Melophorus and Ocymyrmex) and two temperate genera (Formica and Myrmica) to explore convergent and specific adaptations. We found a variable transcriptomic response among desert species exposed to similar levels of physiological heat-stress: Cataglyphis holgerseni and Melophorus bagoti differentially regulated very few transcripts, 0.12% (54/44,525) and 0.14% (53/38,726) respectively, while Cataglyphis bombycina and Ocymyrmex robustior showed greater expression alterations affecting 0.6% (253/41,912) and 1.53% (698/45,701) of their transcriptomes, respectively. These two responsive mechanisms - reactive and constitutive - were related to desert species thermal tolerance survival pattern and convergently evolved in distinct desert ant genera. By comparison, the two temperate species differentially expressed thousands of transcripts more than desert ants in response to heat stress (affecting 8% and 12,71% of F. fusca and Myr. sabuleti transcriptomes), suggesting that keeping restrained gene expression is an important adaptation in heat adapted species. Finally, we found a significant overlap of the molecular pathways activated in response to heat-stress in temperate and desert species, and our data revealed that larger gene expression responses also affected a greater number of taxonomically restricted genes. These results suggest that the molecular processes involved in heat-stress response are mostly evolutionary conserved in ants, but new genes may also play a role.

molecular biology↗

bioRxiv2021

Rapamycin induces autophagy and increases heat tolerance in Drosophila melanogaster

Mechanisms aimed at recovering from heat-induced damage are closely associated with the ability of ectotherms to survive exposition to stressful temperatures. Among these mechanisms the respective contribution of autophagy, a ubiquitous stress-responsive catabolic process, has more recently come to light. By increasing the turnover of cellular structures as well as the clearance of long-lived protein and protein aggregates, the induction of autophagy has been linked to increased tolerance to range of abiotic stressors in diverse ectothermic organisms. Since our understanding of the relationship between autophagy and heat-tolerance currently remains limited in insect models, we hypothesized that (1) heat-stress would cause an increase of autophagy in Drosophila melanogaster tissues and (2) rapamycin exposure would trigger a detectable autophagic response in flies and increase their heat-tolerance. In line with our hypothesis, we report that flies exposed to heat-stress present signs of protein aggregation and appears to trigger an autophagy-related homoeostatic response as a result. We further show that rapamycin feeding causes the systemic effect associated with TOR inhibition, induces autophagy at least locally in the fly gut, and increase the heat-stress tolerance of individuals. This points toward a likely substantial contribution of this autophagy to cope with stressful temperatures in insects.

physiology↗