Abstract. Metabolism provides a basis for using first principles of physics, chemistry, and biology to link the biology of individual organisms to the ecology of populations, communities, and ecosystems. Metabolic rate, the rate at which organisms take up, transform, and expend energy and materials, is the most fundamental biological rate. We have developed a quantitative theory for how metabolic rate varies with body size and temperature. Metabolic theory predicts how metabolic rate, by setting the rates of resource uptake from the environment and resource allocation to survival, growth, and reproduction, controls ecological processes at all levels of organization from individuals to the biosphere. Examples include: (1) life history attributes, including development rate, mortality rate, age at maturity, life span, and population growth rate; (2) population interactions, including carrying capacity, rates of competition and predation, and patterns of species diversity; and (3) ecosystem processes, including rates of biomass production and respiration and patterns of trophic dynamics.Data compiled from the ecological literature strongly support the theoretical predictions. Eventually, metabolic theory may provide a conceptual foundation for much of ecology, just as genetic theory provides a foundation for much of evolutionary biology.

The diversity of life is ultimately generated by evolution, and much attention has focused on the rapid evolution of ecological traits. Yet, the tendency for many ecological traits to instead remain similar over time [niche conservatism (NC)] has many consequences for the fundamental patterns and processes studied in ecology and conservation biology. Here, we describe the mounting evidence for the importance of NC to major topics in ecology (e.g. species richness, ecosystem function) and conservation (e.g. climate change, invasive species). We also review other areas where it may be important but has generally been overlooked, in both ecology (e.g. food webs, disease ecology, mutualistic interactions) and conservation (e.g. habitat modification). We summarize methods for testing for NC, and suggest that a commonly used and advocated method (involving a test for phylogenetic signal) is potentially problematic, and describe alternative approaches. We suggest that considering NC: (1) focuses attention on the withinspecies processes that cause traits to be conserved over time, (2) emphasizes connections between questions and research areas that are not obviously related (e.g. invasives, global warming, tropical richness), and (3) suggests new areas for research (e.g. why are some clades largely nocturnal? why do related species share diseases?).

The latitudinal gradient of increasing biodiversity from poles to equator is one of the most prominent but least understood features of life on Earth. Here we show that species diversity can be predicted from the biochemical kinetics of metabolism. We first demonstrate that the average energy flux of populations is temperature invariant. We then derive a model that quantitatively predicts how species diversity increases with environmental temperature. Predictions are supported by data for terrestrial, freshwater, and marine taxa along latitudinal and elevational gradients. These results establish a thermodynamic basis for the regulation of species diversity and the organization of ecological communities.

Summary1. We present a model that yields ecosystem-level predictions of the flux, storage and turnover of carbon in three important pools (autotrophs, decomposers, labile soil C) based on the constraints of body size and temperature on individual metabolic rate. 2. The model predicts a 10 000-fold increase in C turnover rates moving from tree-to phytoplankton-dominated ecosystems due to the size dependence of photosynthetic rates. 3. The model predicts a 16-fold increase in rates controlled by respiration (e.g. decomposition, turnover of labile soil C and microbial biomass) over the temperature range 0-30 °C due to the temperature dependence of ATP synthesis in respiratory complexes. 4. The model predicts only a fourfold increase in rates controlled by photosynthesis (e.g. net primary production, litter fall, fine root turnover) over the temperature range 0-30 °C due to the temperature dependence of Rubisco carboxylation in chloroplasts. 5. The difference between the temperature dependence of respiration and photosynthesis yields quantitative predictions for distinct phenomena that include acclimation of plant respiration, geographic gradients in labile C storage, and differences between the short-and long-term temperature dependence of whole-ecosystem CO 2 flux. 6. These four sets of model predictions were tested using global compilations of data on C flux, storage and turnover in ecosystems. 7. Results support the hypothesis that the combined effects of body size and temperature on individual metabolic rate impose important constraints on the global C cycle. The model thus provides a synthetic, mechanistic framework for linking global biogeochemical cycles to cellular-, individual-and community-level processes.

4.The fact that quarter-power allometric scaling is so pervasive in biology suggests that different allometric relations have a common, mechanistic origin and provides an empirical basis for theoretical models that derive these scaling exponents.

emissions, yet they are poorly constrained 2,13,14 . There are large uncertainties not only 57 in the current magnitude of these fluxes, but also in the factors that regulate them 2,13 . 58In particular, there is substantial uncertainty in the parameterisation of the 59 temperature dependence of natural CH 4 emissions in process-based biogeochemistry 60 models [15][16][17][18] , which greatly hinders our ability to predict the response of this key 61 component of the carbon cycle to global warming. For example, temperature 62 sensitivities for ecosystem-level CH 4 emissions have reported apparent activation 63 energies that range from 0.2 to 2.5 eV 6,[19][20][21] (1 eV = 96 kJ mol -1 ). 64In a bid to reduce this uncertainty, which is fundamental to improving 65 projections of future carbon cycle-climate change feedbacks 15-18 , we quantified 66 variation in the temperature dependence of CH 4 fluxes for three different types of 67 experiments -i.e. methanogenic cultures, anaerobic sediment slurries, and seasonal 68 field surveys of CH 4 emissions -that correspond to three distinct levels of biological 69 organisation -i.e. population, community, and ecosystem, respectively. In particular, 70 we assess whether ecosystem-level CH 4 emissions exhibit a temperature dependence 71 similar to that of the underlying methanogenic process, and quantify the magnitude of 72 between site deviations from this physiological response. To do this, we first establish 73 the magnitude and variability of the temperature dependence of key metabolic rate 74 processes (i.e. methanogenesis, growth) for populations of methanogens in culture, as 75 well as the temperature dependence of CH 4 production for anaerobic microbial 76 communities in slurries. We then assess whether these temperature dependencies 77 4 differ from those observed in an ecosystem-level analysis of the seasonal temperature 78 dependence of natural CH 4 emissions from aquatic, wetland and rice paddy 79 ecosystems (see S1 of the Supplementary Information). Our ecosystem analysis 80 includes both new and previously published data that together encompass 1553 paired 81 estimates of CH 4 emission and temperature taken from 126 field sites. 82To directly characterise the physiological temperature dependence of key 83 metabolic rate processes for methanogens, we compiled data on rates of 84 methanogenesis and growth from laboratory cultures of methanogen populations as 85 well as rates of CH 4 production from microbial communities in anaerobic sediment 86 slurries (see S1 of the Supplementary Information). We then separately fit the data 87 compiled for each type of experiment to a Boltzmann-Arrhenius function, which 88 characterises the exponential relationship between metabolic rate and temperature 89 assuming a single enzyme catalysed reaction is rate-limiting 22 , using a linear mixed-90 effects model (see S2 of the Supplementary Information) of the form 23 91(1) 92 where is the natural logarithm of the measured rate of CH 4 production or 93 growth rate at absolute tem...

Latitudinal gradients of biodiversity and macroevolutionary dynamics are prominent yet poorly understood. We derive a model that quantifies the role of kinetic energy in generating biodiversity. The model predicts that rates of genetic divergence and speciation are both governed by metabolic rate and therefore show the same exponential temperature dependence (activation energy of Ϸ0.65 eV; 1 eV ‫؍‬ 1.602 ؋ 10 ؊19 J). Predictions are supported by global datasets from planktonic foraminifera for rates of DNA evolution and speciation spanning 30 million years. As predicted by the model, rates of speciation increase toward the tropics even after controlling for the greater ocean coverage at tropical latitudes. Our model and results indicate that individual metabolic rate is a primary determinant of evolutionary rates: Ϸ10 13 J of energy flux per gram of tissue generates one substitution per nucleotide in the nuclear genome, and Ϸ10 23 J of energy flux per population generates a new species of foraminifera. allopatric speciation ͉ biodiversity ͉ macroevolution ͉ metabolic theory of ecology ͉ molecular clock T he latitudinal increase in biodiversity from the poles to the equator is the most pervasive feature of biogeography. For two centuries, since the time of von Humboldt, Darwin, and Wallace, scientists have proposed hypotheses to explain this pattern. New species arise through the evolution of genetic differences among populations from a common ancestral lineage (1-4). Many hypotheses therefore attribute the latitudinal biodiversity gradient to a gradient in speciation rates caused by some independent variable, such as earth surface area or solar energy input (5-7). Some fossil data suggest that speciation rates do indeed increase toward the tropics (8-10), but these findings remain open to debate due in part to our limited understanding of the factors that control macroevolutionary dynamics.Recent advances toward a metabolic theory of ecology (11) provide new opportunities for assessing the factors that control speciation rates. This recent work indicates that two fundamental variables influencing the tempo of evolution, the generation time, and the mutation rate (3) are both direct consequences of biological metabolism (12-14). Here we combine these recent insights from metabolic theory with the theory of population genetics to derive a model that predicts how environmental temperature, through its effects on individual metabolic rates (Eqs. 1-4), influences rates of genetic divergence among populations (Eqs. 5-7) and rates of speciation in communities (Eqs. 8 and 9). We evaluate the model by using data from planktonic foraminifera, because this group has extensive DNA sequence data for evaluating population-level predictions on genetic divergence combined with an exceptionally complete fossil record for evaluating community-level predictions on speciation rates. Model DevelopmentThe two individual-level variables constraining the evolutionary rate of a population, the generation time, and the mutation rate (3) ...

Observations that rates of molecular evolution vary widely within and among lineages have cast doubts on the existence of a single ''molecular clock.'' Differences in the timing of evolutionary events estimated from genetic and fossil evidence have raised further questions about the accuracy of molecular clocks. Here, we present a model of nucleotide substitution that combines theory on metabolic rate with the now-classic neutral theory of molecular evolution. The model quantitatively predicts rate heterogeneity and may reconcile differences in molecular-and fossil-estimated dates of evolutionary events. Model predictions are supported by extensive data from mitochondrial and nuclear genomes. By accounting for the effects of body size and temperature on metabolic rate, this model explains heterogeneity in rates of nucleotide substitution in different genes, taxa, and thermal environments. This model also suggests that there is indeed a single molecular clock mutation ͉ metabolic theory ͉ allometry ͉ substitution C ompletion of the modern evolutionary synthesis will require better understanding of the molecular processes of evolutionary change. The speed of molecular evolution can be measured as the rate of genetic divergence of descendants from a common ancestor, so the rate of molecular evolution can be quantified in terms of the changes in the nucleotide sequences that comprise the genome. Observations that rates of molecular evolution vary widely within and among lineages have raised doubts about the existence of a single ''molecular clock,'' as originally proposed by Zuckerkandl and Pauling (1). The accuracy of molecular clocks is further called into question because molecular estimates of divergence time often disagree with the fossil record (2, 3). Understanding the factors responsible for rate heterogeneity is key to resolving differences between molecular and fossil-based estimates of important evolutionary events [e.g., Cambrian explosion (4, 5) and proliferation of modern mammalian orders (2)]. More generally, understanding rate heterogeneity may yield insight into the factors affecting overall rates of evolution.Variations in rates of nucleotide substitution have been correlated with body size, metabolic rate (6), generation time (7), and environmental temperature (8, 9). Differences also have been observed between endotherms and ectotherms (6, 10). This rate heterogeneity most often is attributed to one of two causes, metabolic rate or generation time. According to the metabolic rate hypothesis, most mutations are caused by genetic damage from free radicals produced as byproducts of metabolism, so mutation rates should be related to cellular or mass-specific metabolic rates (6). According to the generation time hypothesis, most mutations are caused by errors in DNA replication during cell division, so mutation rates should be related to the number of divisions in germ cell lines and hence to generation times (7). Distinguishing between these hypotheses has been difficult because free radical producti...