To understand environmental response at the level of the individual, we investigate phenotypic plasticity. This is a widespread but poorly understood phenomenon whereby a single genotype can produce multiple phenotypes. Epigenetic modifications that regulate cellular plasticity are prime candidates to convey environmental information into ideally suited organismal phenotypes. However, their potential contributions to phenotypic plasticity are still largely unknown. We use the mouth-form polyphenism of Pristionchus pacificus to 1) uncover the identity of epigenetic information carriers that contribute to alternative phenotypes, and (2) determine how these modifications communicate environmental information to transcription, and ultimately physiological and morphological phenotypes.
Relevant Publications:
Jung, J. & Werner, M.S., The histone code at a crossroads: history, context, and new approaches. Trends in Genetics. 2025 [link]]
Reich et al., Developmental transcriptomics in Pristionchus reveals the environmental responsiveness of a plasticity gene-regulatory network. Genome Research. 2025 [link]
Brown et al., Characterization of the Pristionchus pacificus epigenetic toolkit reveals the evolutionary loss of the histone methyltransferase complex PRC2. Genetics. 2023. [link]
Werner et al. Histone 4 lysine 5/12 acetylation enables developmental plasticity of Pristionchus mouth form. Nat Commun. 14, 2095. 2023. [link]
Physiological adaptation to the environment is mediated, at least in part, by gene regulation. Identifying and understanding enhancers and promoters – the DNA sequences which regulate gene expression - has been a major goal of biology in the 21st century. Historically, enhancers and promoters have been treated as distinct, but recent results have led to a sliding scale model. This model builds upon the realization that enhancers and promoters share several molecular features that were once considered unique to one or the other. We are interested in testing this hypothesis, and the potential for enhancer-promoter evolutionary turnover which may contribute to the formation of "new" genes.
Relevant Publications:
Werner, et al.. Young genes have distinct gene structure, epigenetic profiles, and transcriptional regulation. Genome Res. 28, 1675–1687. 2018. [link]
Extremophiles represent the limit of environmental adaptation. The mechanisms which enable survival in extreme environments, like enhanced enzyme stability and unique metabolism, have also been successfully translated to industry. Historically, most of the work on extremophiles has been on microbes; presumably their simpler biology enables greater potential to adapt to extreme environments. However, some animals and plants have found a way to live alongside these single-cell organisms. The comparable lack of extremophile-multicellular-model systems leaves a substantial knowledge gap, and a potential untapped resource for biotechnology.
In 2024 our lab discovered a new species of halophilic nematode in Great Salt Lake, Utah (Diplolaimelloides woaabi). At salinities up to 20%, GSL is among the most saline environments known to harbor animal life. Current projects are investigating D. woaabi to understand the molecular mechanisms, and ecology and evolution of animal adaptation to extreme environments.
Relevant Publications:
Jung et al., "Diplolaimelloides woaabi sp. n. (Nematoda: Monhysteridae): A Novel Species of Free-Living Nematode from the Great Salt Lake, Utah" Journal of Nematology, vol. 57, no. 1, Society of Nematologists, Inc., 2025. [link]
Jung et al., Newly identified nematodes from the Great Salt Lake are associated with microbialites and specially adapted to hypersaline conditions. Proceedings of the Royal Society B. 2024. [link]
Jung et al., Toxic elements in benthic lacustrine sediments of Utah’s Great Salt Lake following a historic low in elevation. Front. Soil Sci., 12 September 2024. Volume 4 - 2024. [link]
Beyond fundamental knowledge, our results may shed light on how our environment (diet, exercise, toxins, etc.) in early stages of life affects long-term health outcomes. For instance, aging and cancer are associated with epigenetic mechanisms of cellular plasticity. Indeed, the same class of chemical inhibitors which affect plasticity are promising chemotherapeutic drugs. A long term goal of our lab is to use experimentally tractable model organisms to identify mechanisms that inform human health and development.