Habitat, latitude and body mass influence the temperature dependence of metabolic rate.

The sensitivity of metabolic rate to temperature constrains the climate in which ectotherms can function, yet the temperature dependence of metabolic rate may evolve in response to biotic and abiotic factors. We compiled a dataset on the temperature dependence of metabolic rate for heterotrophic ectotherms from studies that show a peak in metabolic rate at an optimal temperature (i.e. that describe the thermal performance curve for metabolic rate). We found that peak metabolic rates were lower in aquatic than terrestrial habitats and increased with body mass, latitude and the optimal temperature. In addition, the optimal temperature decreased with latitude. These results support competing hypotheses about metabolic rate adaptation, with hotter being better in the tropics but colder being better towards the poles. Moreover, our results suggest that the temperature dependence of metabolic rate is more complex than previously suggested.

The combined effects of reactant kinetics and enzyme stability explain the temperature dependence of metabolic rates.

A mechanistic understanding of the response of metabolic rate to temperature is essential for understanding thermal ecology and metabolic adaptation. Although the Arrhenius equation has been used to describe the effects of temperature on reaction rates and metabolic traits, it does not adequately describe two aspects of the thermal performance curve (TPC) for metabolic rate-that metabolic rate is a unimodal function of temperature often with maximal values in the biologically relevant temperature range and that activation energies are temperature dependent. We show that the temperature dependence of metabolic rate in ectotherms is well described by an enzyme-assisted Arrhenius (EAAR) model that accounts for the temperature-dependent contribution of enzymes to decreasing the activation energy required for reactions to occur. The model is mechanistically derived using the thermodynamic rules that govern protein stability. We contrast our model with other unimodal functions that also can be used to describe the temperature dependence of metabolic rate to show how the EAAR model provides an important advance over previous work. We fit the EAAR model to metabolic rate data for a variety of taxa to demonstrate the model's utility in describing metabolic rate TPCs while revealing significant differences in thermodynamic properties across species and acclimation temperatures. Our model advances our ability to understand the metabolic and ecological consequences of increases in the mean and variance of temperature associated with global climate change. In addition, the model suggests avenues by which organisms can acclimate and adapt to changing thermal environments. Furthermore, the parameters in the EAAR model generate links between organismal level performance and underlying molecular processes that can be tested for in future work.

Quantitative trait loci and interaction effects responsible for variation in female postmating mortality in Drosophila simulans and D. sechellia introgression lines.

Mating appears to inflict a cost to Drosophila females, resulting in a reduction of their lifespan shortly after mating. Males from different chromosome extracted lines differ significantly in their detrimental effects on postmating female survival, and seminal fluid proteins produced in the male accessory glands are at least partially responsible for the effect. This suggests that there is a genetic basis underlying the male inflicted effect on female's postmating mortality. However, the genes responsible for this effect remain elusive. Using males from introgression lines between D. simulans and D. sechellia genomes and a quantitative trait locus (QTL) mapping approach, we identified chromosomal regions that affect postmating mortality of females. We found a second chromosome QTL with an effect on average female lifespan after mating and a third chromosome QTL with an effect on postmating female mortality rate. Under the general observation of a faster divergence of sex-related genes among closely related species, it is predicted that genes for reproductive traits other than hybrid sterility will show evidence of epistatic effects when brought into a heterospecific background. We detected a significant epistatic genetic effect on postmating female mortality rate that supports this prediction.