Matthew D. Hall

The time it takes organisms to reach adulthood is often considered a central life-history trait that influences fitness and is highly plastic across environments. Despite its importance, direct estimates of how selection on development time varies across combinations of environmental stressors remain rare, limiting our understanding of its role in population responses to environmental change. We reared 68 full-sibling families of the vinegar fly, Drosophila melanogaster , at two temperatures (14°C and 28°C) on two diets (standard and low-calorie), and measured development time, body size (mass and wing size), egg-to-adult viability and productivity (number of offspring). Temperature caused the largest plastic response, with development taking 4–5 times longer at 14°C, whereas the low-calorie diet extended development by 20–30%. Yet diet, not temperature, changed directional selection on development time. On the standard diet, faster development was associated with higher fitness at both temperatures. On the low-calorie diet, this advantage disappeared, and at 14°C slower-developing females tended to produce more offspring. Viability selection showed consistent patterns. The low-calorie diet also increased evolvability in development time c.10–16-fold at both temperatures, and genetic correlations between diets were close to zero, indicating strong genotype-by-environment interactions. Plasticity in development time was not associated with fitness in any treatment. Overall, we provide evidence that development time is a functional trait whose relationship with fitness depends on the environment. Nutritional stress induced a smaller plastic response in development time than temperature, but had a larger effect on directional selection and evolvability. The stressor causing the greatest plastic change in a functional trait is therefore not necessarily the one that shapes its selection and evolution.

The thermal environment can profoundly modify the damage that pathogens cause to hosts. Yet while the interacting impacts of infection and temperature on individual life‐history traits are well documented, how these effects scale to demographic consequences across thermal gradients remains poorly understood. Using the Daphnia magna–Pasteuria ramosa system across a 10–30°C gradient, we tested whether virulence in individual‐level life history metrics reliably reflects the consequences for predicted population growth rates. Our results reveal a stark mismatch between scales: the cost of infection on individual life‐history traits (fecundity, body size, and lifespan) was maximised at low temperatures, whereas the impact on population growth rate was maximised at high temperatures and at the thermal optima of healthy hosts. These findings demonstrate that standard virulence metrics at the scale of individual life‐history traits may underestimate demographic risk in warming environments. To reliably predict population persistence in the face of disease under a changing climate, it is important to account for the temperature‐dependent scaling of pathogen virulence and host life‐history to population growth rates.

Sex differences in thermal tolerance may significantly impact population responses to climate change, yet most studies examining geographic variation in thermal tolerance focus on a single sex. Here, we investigate how males and females might vary in their capacity to tolerate the heat along a latitudinal cline using the Australian water flea, Daphnia carinata. We measured heat knockdown times in males and females using clones of Daphnia from six populations spanning eastern Australia, raised under two acclimation temperatures (20°C and 25°C). Females consistently showed higher thermal tolerances than males, with greater capacity for thermal acclimation. Critically, we discovered that latitudinal clines in thermal tolerance were sex-specific: females showed a much steeper decline in heat tolerance with increasing latitude compared with males. As a result, sexual dimorphism in thermal tolerance was more than twice as large in northern populations compared with southern populations. These results suggest that sex-specific selection, potentially driven by differential habitat use or the female-biased demography of cyclical parthenogenesis, may be driving divergent thermal adaptation between the sexes. Our findings highlight the importance of considering both sexes when predicting population vulnerability to climate change, as sex-averaged estimates may misrepresent the heat tolerance of populations along environmental gradients.

Latitudinal clines are routinely used as evidence of adaptation across broad climatic gradients. However, if environmental variation influences the strength of latitudinal clines, then clinal patterns will be unstable, and using patterns of adaptation to predict population responses to global change will be difficult. To test whether environmental variation influences latitudinal clines, we sampled five populations of Drosophila melanogaster spanning 3000 km of east coast Australia, and measured stress tolerance (heat, cold and desiccation) and body size on flies that developed in six combinations of temperature (13°C, 25°C and 29°C) and diet (standard and low-calorie) treatments. We found latitudinal clines where populations further from the equator had larger wings, higher cold tolerance and lower heat tolerance. For all traits, temperature determined the strength of latitudinal clines, whereas diet had little influence. Steeper clines often emerged in warmer treatments, created by latitudinal clines in plasticity. In the warmest temperature, higher latitude populations showed larger increases in heat tolerance, larger reductions in desiccation tolerance but smaller decreases in cold tolerance. Heat tolerance was the only trait that supported the climate variability hypothesis and a trade-off between plasticity and tolerance. Environment-dependent latitudinal clines are therefore likely to determine variation in population responses to global change.

While climate adaptation is typically quantified across broad gradients, the potential for adaptation to the same environmental variables at small scales is rarely tested. If local-scale environmental heterogeneity can generate patterns of adaptation similar to broad gradients, then we currently underestimate adaptive capacity to global change. We quantified population variation in climate tolerance traits and their plasticity for five populations of Drosophila melanogaster from a 3000-km latitudinal gradient, which we contrasted with eight local populations from an environmentally heterogeneous 600×300km area. Population variation in stress tolerance at the local scale was comparable to that across latitude. Consistent with local adaptation, populations from warmer and drier environments showed greater heat and desiccation tolerance, and populations from more predictable environments showed greater plasticity. Climate adaptation at smaller geographic scales can therefore be comparable to adaptation across broad geographic scales. However, patterns of adaptation often changed across geography, which makes predicting responses to global change challenging.

Latitudinal clines are routinely used as evidence of adaptation across broad climatic gradients. However, if environmental variation influences the strength of latitudinal clines, then clinal patterns will be unstable, and using patterns of adaptation to predict population responses to global change will be difficult. To test whether environmental variation influences latitudinal clines, we sampled five populations of Drosophila melanogaster spanning 3000-km of east coast Australia, and measured stress tolerance (heat, cold and desiccation) and body size on flies that developed in six combinations of temperature (13°C, 25°C and 29°C) and diet (standard and low-calorie) treatments. We found latitudinal clines where populations further from the equator had larger wings, higher cold tolerance and lower heat tolerance. For all traits, temperature determined the strength of latitudinal clines, whereas diet had little influence. Steeper clines often emerged in warmer treatments, created by latitudinal clines in plasticity. In the warmest temperature, higher latitude populations showed larger increases in heat tolerance, larger reductions in desiccation tolerance but smaller decreases in cold tolerance. Heat tolerance was the only trait that supported the climate variability hypothesis and a trade-off between plasticity and tolerance. Environment-dependent latitudinal clines are therefore likely to determine variation in population responses to global change.

The incidence of arboviral diseases like dengue, chikungunya, and yellow fever continues to rise in association with the expanding geographic ranges of their vectors, Aedes aegypti and Aedes albopictus. The distribution of these vectors is believed to be driven in part by climate change and increasing urbanization. Arboviruses navigate a wide range of temperatures as they transition from ectothermic vectors (from 15°C to 35°C) to humans (37°C) and back again, but the role that temperature plays in driving the evolution of arboviruses remains largely unknown. Here, we passaged replicate dengue serotype-2 virus populations 10 times at either 26°C (Low) or 37°C (High) in C6/36 Aedes albopictus cells to explore the differences in adaptation to these thermal environments. We then deep-sequenced the resulting passaged dengue virus populations and tested their replicative fitness in an all-cross temperature regime. We also assessed the ability of the passaged viruses to replicate in the insect vector. While viruses from both thermal regimes accumulated substitutions, only those reared in the 37°C treatments exhibited nonsynonymous changes, including several in the E, or envelope protein, and multiple non-structural genes. Passaging at the higher temperature also led to reduced replicative ability at 26°C in both cells and mosquitoes. One of the mutations in the E gene involved the loss of a glycosylation site previously shown to reduce infectivity in the vector. These findings suggest that viruses selected for growth at higher ambient temperatures may experience tradeoffs between thermostability and replication in the vector. Such associations might also have implications for the suitability of virus transmission under a changing climate.

Sex differences are predicted to play an important role in the spread and evolution of pathogens. However, attempts to generalize the ‘sicker’ sex have been challenged by intraspecific variability of sex-biases across the infection process. Sex specific plasticity provides a framework to resolve this by elucidating how infection is shaped at the sex-pathogen-environment interface. Using the Daphnia magna and Pasteuria ramosa system, we measure infection outcomes for males and females across three temperatures and seven pathogen densities to quantify how sex specific plasticity shapes susceptibility, pathogen loads, and ultimately transmission. We find unique forms of plasticity at each stage of infection – including equivalent, sex-specific, and divergent plasticity. Integrating these into a single estimate of transmission reveals a clear pattern – male-biased transmission at cold temperatures, and female-biased transmission at warm temperatures. Sex specific thermal plasticity thus determines the ‘sicker’ sex, with implications for pathogen spread and evolution in a warming world.

A suite of plant traits is thought to make weed populations highly invasive, including vigorous growth and reproduction, superior competitive ability, and high dispersal ability. Using a breeding design and a common garden experiment, we tested whether such an “invasion syndrome” has evolved in an invasive range of Solidago altissima, and whether the evolution is likely to be genetically constrained. We found an overall shift in invasive phenotypes between native North American and invasive Japanese populations. The invasive populations were taller and produced more leaves, suggesting a superior ability to exploit limited resources. The populations also produced more allelopathic compounds that can suppress competitor growth. Finally, invasive populations produced more seeds, which are smaller and are released from a greater height, indicating a potential for superior dispersal ability than the native populations. Quantitative genetics analyses found a large amount of additive genetic variation in most focal traits across native and invasive populations, with no systematic differences in its magnitude between the ranges. Genetic covariances among three traits representing invasion strategies (leaf mass, polyacetylene concentration and seed size) were small. The R metric, which measures the effect of genetic covariances on the rate of adaptation, indicated that the covariance neither constrains nor accelerates concerted evolution of these traits. The results suggest that the invasion syndrome in S. altissima has evolved in the novel range due to ample additive genetic variation, and relatively free from genetic trade‐offs.