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Nels C. Elde

Assistant Professor of Human Genetics

B.A. Carleton College

Ph.D. University of Chicago

Research

References

nelde@genetics.utah.edu

Nels Elde's Lab Page

Nels Elde's PubMed Literature Search

Research

We study the evolution of conflict. Host-pathogen interactions are hotspots of genetic conflict and battlefronts for influence over host functions. From an evolutionary perspective each interaction can weigh heavily on the survival of both hosts and pathogens. Therefore, these interactions drive some of the most dramatic adaptations and rapid evolution found in nature. We use host-pathogen interfaces as model systems for studying the evolutionary process.

A key evolutionary strategy is mimicry. Mimicry provides evolutionary gains in many situations; from rainforest butterflies disguised as poisonous species down to the molecular interface of host-pathogen interactions. Mimics encoded by viruses interfere with a variety of host functions. Our lab uses evolutionary and experimental approaches with diverse panels of primate cell lines to investigate host-mimic evolution. One example is the interaction between the anti-viral Protein kinase R and a mimic of its substrate encoded by poxviruses. These studies are revealing mechanisms of self-recognition at protein-protein interfaces and raising new questions about the evolutionary dynamics of mimicry.

Host-pathogen interfaces often evolve in ways that resemble arms races. This phenomenon of genetic conflict has been described by the Red Queen hypothesis, which posits that opposing entities vie for dominance in seesawing battles of ongoing adaptations. In the lab we use extensive phylogenetic analysis to identify and study molecular arms races involving host immunity factors and antagonistic proteins encoded by pathogens.

In addition to host evolution, we study the evolution of large DNA viruses, such as vaccinia, the model poxvirus. While experiments based on phylogenetic reconstructions provide a powerful means of retrospectively studying host-pathogen interactions, experimental evolution offers a prospective view of virus evolution where adaptations can be monitored in real-time. Recent advances in deep genome sequencing coupled with recombinant tools make possible to quickly determine the genetic basis of a variety of adaptations. We are using experimental evolution of vaccinia to decipher mechanisms of virus adaptation, such as host switching, which in the wild can lead to new epidemics.

 

A swallowtail butterfly next to the crystal structure
of a virus-encoded mimic of a kinase substrate.

 

References