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Whether populations can adapt to predicted climate change conditions, and how rapidly, are critical questions for the management of natural systems. Experimental evolution has become an important tool to answer these questions. In order to provide useful, realistic insights into the adaptive response of populations to climate change, there needs to be careful consideration of how genetic differentiation and phenotypic plasticity interact to generate observed phenotypic changes. We exposed three populations of the widespread copepod Acartia tonsa (Crustacea) to chronic, sublethal temperature selection for 15 generations. We generated thermal survivorship curves at regular intervals both during and after this period of selection to track the evolution of thermal tolerance. Using reciprocal transplants between ambient and warming conditions, we also tracked changes in the strength of phenotypic plasticity in thermal tolerance. We observed significant increases in thermal tolerance in the Warming lineages, while plasticity in thermal tolerance was strongly reduced. We suggest these changes are driven by a negative relationship between thermal tolerance and plasticity in thermal tolerance. Our results indicate that adaptation to warming through an increase in thermal tolerance might not reduce vulnerability to climate change if the increase comes at the expense of tolerance plasticity. These results illustrate the importance of considering changes in both a trait of interest and the trait plasticity during experimental evolution.

Alterations in fish developmental trajectories occur in response to genetic and environmental changes, especially during sensitive periods of development (critical windows). Embryos and larvae of Atractosteus tropicus were used as a model to study fish survival, growth, and development as a function of temperature (28 °C control, 33 °C, and 36 °C), salinity (0.0 ppt control, 4.0 ppt, and 6.0 ppt), and air saturation (control ~95% air saturation, hypoxia ~30% air saturation, and hyperoxia ~117% air saturation) during three developmental periods: (1) fertilization to hatch, (2) day 1 to day 6 post hatch (dph), and (3) 7 to 12 dph. Elevated temperature, hypoxia, and hyperoxia decreased survival during incubation, and salinity at 2 and 3 dph. Growth increased in embryos incubated at elevated temperature, at higher salinity, and in hyperoxia but decreased in hypoxia. Changes in development occurred as alterations in the timing of hatching, yolk depletion, acceptance of exogenous feeding, free swimming, and snout shape change, especially at high temperature and hypoxia. Our results suggest identifiable critical windows of development in the early ontogeny of A. tropicus and contribute to the knowledge of fish larval ecology and the interactions of individuals × stressors × time of exposure.

Recent experiments suggest that timing of metamorphosis is fixed during development in some anurans, insects, and freshwater invertebrates. Yet, these experiments do not exclude a growth rate optimization model for the timing of metamorphosis. I manipulated food resources available to larvae of squirrel treefrogs (Hyla squirella) to determine if there is a loss of plasticity in duration of larval period during development and to critically test growth rate models for the timing of metamorphosis. Size-specific resource levels for individual tadpoles were switched from low to high or high to low at three developmental stages spaced throughout larval development. The effects of changes in resource availability on larval period and mass at metamorphosis were measured. Switching food levels after late limb bud development did not significantly affect larval period in comparison to constant food level treatments. Therefore, developmental rate in H. squirella is better described by a fixed developmental rate model, rather than a growth rate optimization model. The timing of fixation of developmental rate in H. squirella is similar to that found in other anuran species, suggesting a taxonomically widespread developmental constraint on the plasticity of larval period duration. Mass at metamorphosis was not significantly affected by the timing of changes in food levels; the amount of food available later in development determined the size at metamorphosis. Larval period and mass at metamorphosis were negatively correlated in only one of two experiments, which contrasts with the common assumption of a phenotypic trade-off between decreased larval period and increased mass at metamorphosis.

Hormones are chemical signaling molecules that regulate patterns of cellular physiology and gene expression underlying phenotypic traits. Hormone-signaling pathways respond to an organism’s external environment to mediate developmental stage-specific malleability in phenotypes, so that environmental variation experienced at different stages of development has distinct effects on an organism’s phenotype. Studies of hormone-signaling are therefore playing a central role in efforts to understand how plastic phenotypic responses to environmental variation are generated during development. But, how do adaptive, hormonally mediated phenotypes evolve if the individual signaling components (hormones, conversion enzymes, membrane transporters, and receptors) that comprise any hormone-signaling pathway show expressional flexibility in response to environmental variation? What relevance do these components hold as molecular targets for selection to couple or decouple correlated hormonally mediated traits? This article explores how studying the endocrine underpinnings of phenotypic plasticity in an ecologically relevant context can provide insights into these, and other, crucial questions into the role of phenotypic plasticity in evolution, including how plasticity itself evolves. These issues are discussed in the light of investigations into how thyroid hormones mediate morphological plasticity in Death Valley’s clade of pupfishes (Cyprinodon spp.). Findings from this work with pupfish illustrate that the study of hormonesignaling from an ecological perspective can reveal how phenotypic plasticity contributes to the generation of phenotypic novelty, as well as how physiological mechanisms developmentally link an organism’s phenotype to its environmental experiences.

Understanding how populations respond to rapid environmental change is critical both for preserving biodiversity and for human health. An increasing number of studies have shown that genetic variation that has no discernable effect under common ecological conditions can become amplified under stressful or novel conditions, suggesting that environmental change per se can provide the raw materials for adaptation. Indeed, the release of such hidden, or “cryptic,” genetic variants has been increasingly viewed as playing a general and important role in allowing populations to respond to rapid environmental change. However, additional studies have suggested that there is a balance between cryptic genetic variants that are potentially adaptive in future environments and genetic variants that are deleterious. In this article, we begin by discussing how population and environmental parameters—such as effective population size and the historical frequency and strength of selection under inducing conditions—influence relative amounts of cryptic genetic variation among populations and the overall phenotypic effects of such variation. The amount and distribution of cryptic genetic variation will, in turn, determine the likelihood that cryptic variants, once expressed, will be adaptive or maladaptive during environmental transitions. We then present specific approaches for measuring these parameters in natural populations. Finally, we discuss one natural system that will be conducive to testing whether populations that vary in these parameters harbor different amounts, or types, of cryptic genetic variation. Generally, teasing apart how population and environmental parameters influence the accumulation of cryptic genetic variation will help us to understand how populations endure and adapt (or fail to adapt) to natural environmental change and anthropogenic disturbance.

Variable environmental conditions can alter the phenotype of offspring, particularly in ectothermic species such as reptiles. Despite this, the majority of studies on development in reptiles have been carried out under constant conditions in the laboratory, raising the question of just how applicable those investigations are to natural conditions? Here, we first review what we have learned from these constant-temperature studies. Second, we examine the importance of temperature fluctuations for development in reptiles and highlight the outcomes of studies conducted under fluctuating conditions. Next, we report our findings from a new study that examines how the frequency of fluctuations in temperature experienced during development affects phenotype. Finally, we suggest some areas in need of additional research so that we can better understand the complex interactions of temperature and physiology, particularly in species with temperature-dependent sex determination. For questions aimed at understanding the complex effects of the environment on phenotype, we must move toward studies that better capture environmental variation. By taking such an approach, it may be possible to predict more accurately how these thermally sensitive organisms will respond to environmental perturbations, including climatic change.

Rising temperatures associated with global climatic change threaten the persistence of species. Determining how species adapt to environmental change is paramount. Much work has shown that environmental stressors have the potential to induce phenotypic changes that span multiple generations. Such transgenerational plasticity (TGP) represents a mechanism that may allow for rapid responses to global climatic change. Yet, our understanding of thermal TGP beyond the relationship between parent and offspring is limited. We evaluated thermal TGP in development across three generations (i.e., F₀, F₁, and F₂) in zooplankton (Daphnia ambigua) from lakes in Connecticut. We found that the temperatures at which parents and grandparents were reared significantly influenced age at maturation in the grandoffspring. Comparisons between the F₀ and F₁ generation show that the offspring of parents reared at low temperatures matured significantly faster than the offspring of parents reared at a higher temperature. However, age at maturation in the grand-offspring was influenced by the interactive effects of parents and grandparents. Such an effect yielded trends that were not readily predicted from the previous generations and whose adaptive significance is unclear. Our results thus call for additional theoretical and empirical work to better understand the transgenerational effects of temperature.

Diverse subfields of biology have addressed phenotypic plasticity, but have emphasized different aspects of the definition, thereby shaping the questions that are asked and the methodological approaches that are employed. A key difference between studies of plasticity in the fields of evolutionary biology and physiology is the degree of focus upon the contribution of genetic variance to plastic traits. Although evolutionary biology is generally focused on the heritability and adaptive value of plastic traits and therefore the potential for plasticity to impact changes in traits across generations, physiological studies have historically focused on the timing and reversibility of plastic change across seasons or ages and the mechanisms underlying traits’ plasticity. In this review and the symposium from which it emerged, we aimed to highlight ways that integrative biologists can better communicate about their research and design better studies to address phenotypic plasticity. Evolutionary theory clarifies the need to assess fitness using reliable measures, such as survival and reproductive success, and to consider the heritability and genetic variance underlying plasticity. Reciprocally, physiological research demonstrates that understanding the mechanisms that permit, or limit, plasticity, whether through pleiotropic effects, developmental, or functional linkages between traits, or epigenetic modifications, will shed light on limitations to phenotypic plasticity. Uniting the fields of evolution and physiology to address all aspects of phenotypic plasticity will be increasingly important as the rate of anthropogenic environmental change increases and biologists must predict the responses of wild populations to novel environments, as well as determine the most effective conservation interventions.

Behavioral, hormonal, and genetic processes interact reciprocally, and differentially affect behavior depending on ecological and social contexts. When individual differences are favored either between or within environments, developmental plasticity would be expected. Parental effects provide a rich source for phenotypic plasticity, including anatomical, physiological, and behavioral traits, because parents respond to dynamic cues in their environment and can, in turn, influence offspring accordingly. Because these inter-generational changes are plastic, parents can respond rapidly to changing environments and produce offspring whose phenotypes are well suited for current conditions more quickly than occurs with changes based on evolution through natural selection. I review studies on developmental plasticity and resulting phenotypes in Belding’s ground squirrels (Urocitellus beldingi), an ideal species, given the competing demands to avoid predation while gaining sufficient weight to survive an upcoming hibernation, and the need for young to learn their survival behaviors. I will show how local environments and perceived risk of predation influence not only foraging, vigilance, and anti-predator behaviors, but also adrenal functioning, which may be especially important for obligate hibernators that face competing demands on the storage and mobilization of glucose. Mammalian behavioral development is sensitive to the social and physical environments provided by mothers during gestation and lactation. Therefore, maternal effects on offspring’s phenotypes, both positive and negative, can be particularly strong.

Colonization of novel environments can alter selective pressures and act as a catalyst for rapid evolution in nature. Theory and empirical studies suggest that the ability of a population to exhibit an adaptive evolutionary response to novel selection pressures should reflect the presence of sufficient additive genetic variance and covariance for individual and correlated traits. As correlated traits should not respond to selection independently, the structure of correlations of traits can bias or constrain adaptive evolution. Models of how multiple correlated traits respond to selection often assume spatial and temporal stability of trait-correlations within populations. Yet, trait-correlations can also be plastic in response to environmental variation. Phenotypic plasticity, the ability of a single genotype to produce different phenotypes across environments, is of particular interest because it can induce population-wide changes in the combination of traits exposed to selection and change the trajectory of evolutionary divergence. We tested the ability of phenotypic plasticity to modify trait-correlations by comparing phenotypic variance and covariance in the bodyshapes of four experimental populations of Trinidadian guppies (Poecilia reticulata) to their ancestral population. We found that phenotypic plasticity produced both adaptive and novel aspects of body-shape, which was repeated in all four experimental populations. Further, phenotypic plasticity changed patterns of covariance among morphological characters. These findings suggest our ability to make inferences about patterns of divergence based on correlations of traits in extant populations may be limited if novel environments not only induce plasticity in multiple traits, but also change the correlations among the traits.