Overview
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Imagine that you had an identical twin--with the same DNA sequence--and your twin only ate cake, and you only ate salad. It is highly likely that the two of you would look, feel, and maybe even act differently because of these diet choices--even though you have the same genome. This points to a central theme of our lab's work: phenotypes are not wrought by genes alone.

The ultimate source of phenotypic variation is developmental innovation, which depends on genetic and environmental factors. Nowhere is this point more apparent than by the widespread existence of a phenomenon known as ‘phenotypic plasticity,’ which is the ability of organisms to produce multiple phenotypes in response to environmental variation. Our research strives to understand how genes and environment influence phenotype production within and between generations by investigating the developmental, ecological, and evolutionary causes and consequences of phenotypic plasticity.

Like you and your twin in the example above, many animals with identical, or very similar, genomes consume different resources. In some extreme cases, these differences in diet can cause them to develop into essentially different creatures. We use these extreme cases as models for our work. That is, we focus on studying resource polyphenism—the occurrence of environmentally induced discrete intraspecific morphs showing differential niche use. This form of plasticity is particularly interesting because it acts as a nexus for integrating intra- and interspecific species interactions with metabolic and molecular developmental mechanisms of plasticity. More generally, the study of resource polyphenism feeds into diverse fields ranging from molecular biology to community ecology and has led our explorations into the ecological, evolutionary, and molecular origins of novelty, diversity, and adaptation.

By leveraging the strengths of diverse taxa, such as diplogastrid nematodes and spadefoot toad tadpoles (Gallery), we are addressing important questions about phenotypic plasticity at various levels of biological organization. 

Although we are interested in all questions related to the themes above, our current foci include:
      1) Uncovering plasticity's molecular bases in a complex natural system
      2) Determining how constraints on plasticity affect its evolution
      3) Clarifying how nongenetic inheritance influences the evolution of plasticity
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Uncovering plasticity's molecular bases in a complex natural system
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We are using environmental manipulations, transcriptomics, and functional genetics (via CRISPR/Cas9) on candidate genes and pathways to interrogate the molecular mechanisms of spadefoot tadpole resource polyphenism. The goal of these studies is to unravel the regulatory interactions needed to produce carnivore morph tadpoles. Subsequently, we plan to also explore how such interactions have evolved and diverged among spadefoot lineages, including those that never evolved plasticity and those that have secondarily lost it. This work brings a well-developed system for studying evolutionary ecology into the realm of functional genetics and provides much-needed mechanistic details of plasticity evolution in nature.
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Determining how constraints on plasticity affect its evolution
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Costs and limits to plasticity are key drivers of genetic assimilation (the evolutionary loss of plasticity). Yet, the mechanistic bases and molecular underpinnings of these constraints are generally unknown. This research program aims to disentangle these issues by integrating multifactorial and multigenerational experiments across diverse lineages of shark-tooth nematodes (including those that have lost plasticity and/or reproduce by selfing) with functional manipulation of the polyphenism gene network (e.g., so-called “sensors”, “modulators”, and “effectors”). We seek to the determine genetic and environmental contexts that favor/disfavor plasticity compared to constitutive expression or incomplete phenotype production. These efforts address a key empirical challenge in the field, namely, how costs and limits of plasticity contribute to the evolution and development of polyphenism. Further, they will inform how plasticity influences diversification within and among species.
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Clarifying how nongenetic inheritance influences the evolution of plasticity
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Theory suggests that epigenetic mechanisms and nongenetic inheritance, because they might offer a bridge to genetically inherited change, should be key factors in facilitating genetic assimilation. Using both nematodes and spadefoot toads, we are following up on previous efforts to empirically understand if, when, and how, nongenetic inheritance facilitates the evolution (and potentially the loss) of plasticity and how such inheritance is linked to genetically mediated evolution. This work will integrate diverse approaches from landscape genetics and mesocosm experiments to functional manipulation of target regulators via CRISPR/Cas9 under alternative environmental conditions. In general, these studies will give a mechanistic face to longstanding theory on the interplay between nongenetic inheritance, plastic development, and plasticity evolution.