Research Interests

My general interests are in theoretical population biology and evolutionary ecology. The research typically combines modeling, mathematics, and simulations, and is usually in collaboration with experimental biologists. I am especially interested in the interface between theory, modeling, and empirical ecology, and using dynamic models as a tool for identifying the mechanisms that drive the dynamics of ecological systems. I believe that useful theory must be grounded in real data, and must prove itself by leading to greater understanding of empirical results.

 

If my research group had a motto, it might be (paraphrasing Benjamin Franklin): "Nothing is certain but predators and parasites". Nature abhors an uneaten meal, so the fundamental links in ecosystems are between organisms and the other organisms that try to consume them all at once (predators) or slowly (parasites). Our other motto might be "Evolution changes everything". These are not unrelated. Becoming somebody else's dinner, or being turned into a factory for producing the next generation of Plasmodium (the protozoan that causes malaria), are very strong natural selection. It is hard to imagine these events occurring without significant evolutionary consequences. But exactly that thinking is embedded in most of the ecological theory underpinning environmental and natural resource management. Models for host-pathogen dynamics have started to include pathogen evolution, but still ignore host evolution. We need broadened theories that let us take account of the fact that we are studying and managing a moving target.

My current projects include:

1. Ecology and Evolution in an Experimental Predator-prey System (1997-present)

For about a decade we have trying to understand the mechanisms driving population dynamics in a simple experimental system: a chemostat (flow-through glass vessel) in which predators (rotifers) consume prey (algae) who require a limiting nutrient (N supplied as nitrate) that is supplied in the inflowing culture medium. This was our introduction to the importance of rapid evolution and how it could literally "change everything" about one of the most classic (and "well understood") phenomena in ecology: predator-prey cycles.

Research support 

*       Evaluating Complex Dynamics and Chaos in Natural Ecological Systems: Experimental, Statistical, and Modeling Approaches (co-PI Nelson G. Hairston, Jr.), Andrew W. Mellon Foundation, 1997- 2002.

*       The Evolutionary Ecology of Population Dynamics: Experimental  and Modeling Approaches (co-PI Nelson G. Hairston, Jr.), Andrew W. Mellon Foundation, 2003-2007.

*       Contemporary Rapid Evolution: Dynamics and Persistence in Complex Ecological Communities (co-PIs Nelson G. Hairston, Jr., Laura E. Jones, and G.F. Fussmann), James S McDonnell Foundation, 2008-2011.

 

 

 


Selected Publications

2007  

*       T. Yoshida, S. P. Ellner, L. E. Jones, B. J. M. Bohannan, R. E. Lenski, N. G. Hairston Jr. 2007. Cryptic population dynamics: rapid evolution masks trophic interactions. PloS Biology 5: e235.  doi:10.1371/journal.pbio.0050235

*       L.E. Jones and S.P. Ellner. Effects of rapid prey evolution on predator-prey cycles. Journal of Mathematical Biology 55:541–573.

2006

*       J.R. Meyer, Stephen P. Ellner, Nelson G. Hairston, Jr., Laura E. Jones, and Takehito Yoshida. Prey evolution on the time scale of predator–prey dynamics revealed by allele-specific quantitative PCR. Proceedings of the National Academy of Sciences 103: 10690–10695.

2005

*       Gregor F. Fussman, Stephen P. Ellner, Nelson G. Hairston, Jr., Laura E. Jones, Kyle W. Shertzer and Takehito Yoshida. Ecological and evolutionary dynamics of experimental plankton communities. Advances in Ecological Research 37: 221-243. 

*       N. G. Hairston, Jr., S. P. Ellner, M. A. Geber, T. Yoshida, and J. A. Fox. Rapid evolution and the convergence of ecological and evolutionary time. Ecology Letters 8: 1114-1127.

2004

*       L.E. Jones and S.P. Ellner. Evolutionary tradeoff and equilibrium in an aquatic predator-prey system. Bulletin of Mathematical Biology 66: 1547-1573.

*       T.Y. Yoshida, N.G. Hairston, Jr., and S.P. Ellner. Evolutionary tradeoff between defence against grazing and competetive ability in a simple unicellular alga, Chlorella vulgaris. Proceedings of the Royal Society of London Series B 271: 1947 - 1953. 

2003

*       T. Yoshida, L.E. Jones, S.P. Ellner, G.F. Fussmann, and N. G. Hairston, Jr. Rapid evolution drives ecological dynamics in a predator-prey system. Nature 424: 303-306.

*       G. F. Fussmann, S.P. Ellner, and N.G. Hairston, Jr. Evolution as a critical component of plankton dynamics. Proceedings of the Royal Society of London Series B 270: 1015-1022.

*       S.P. Ellner and G.F. Fussmann. Effects of successional dynamics on metapopulation persistence. Ecology, 84: 882–889.

2002

*       G. F. Fussmann and G. Heber. Food web complexity and chaotic population dynamics. Ecology Letters 5: 394-401.

*       S. P. Ellner, Y. Seifu, and Robert H. Smith. Fitting population models to time series data by gradient matching. Ecology 83: 2256-2270.  

*       K.W. Shertzer and S.P. Ellner. Energy storage and the evolution of population dynamics. Journal of Theoretical Biology 215: 183–200.

*       K.W. Shertzer and S.P. Ellner. State-dependent energy allocation in variable environments: life history evolution of a rotifer. Ecology 83: 2181–2193.

*       K. W. Shertzer, S.P. Ellner, G.F. Fussmann, and N.G. Hairston, Jr. Predator-prey cycles in an aquatic microcosm: testing hypotheses of mechanism. Journal of Animal Ecology 71: 802–815.

2001

*       P. Schliekelman and S.P. Ellner. Egg size evolution and energetic constraints on population dynamics. Theoretical Population Biology 60: 73-92.

2000

*       G. F. Fussmann, S.P. Ellner, K.W. Shertzer, and N.G. Hairston, Jr. Crossing the Hopf bifurcation in a live predator-prey system. Science 290: 1358-1360.

 

Origins and Spread of the Aspergillus-Gorgonian Coral Epizootic: Role of Climate and Environmental Facilitators (2003-2007)

This multi-investigator, multi-instutution project, was funded by NSF under the "Ecology of Infectious Diseases" program. Other participants at Cornell are C. Drew Harvell (PI), Laura Jones (Research Associate), and Laura Mydlarz (University of Texas Arlington). 

Coral reefs worldwide have seen major declines in recent decades, and infectious diseases are one of the most important factors in this decline. Aspergillosis is a fungal pathogen affecting seafan corals in the Caribbean, causing up to 90% local mortality. We will be using the epizootic as a model system for testing hypotheses about the origins and spread of emergent marine diseases. The recent high rates of coral disease outbreaks may be caused by climate-related and other anthropogenic environmental stresses such as marine eutrophication, increased inputs of new pathogens, or both. Traditional methods of disease management (such as culling, vaccination, quarantine) cannot be used in marine systems, which adds urgency to understanding and controlling disease in the ocean. The most practical remediation is to control inputs and spread, but we rarely know the origin of any coral pathogen, nor do we understand mechanisms of transmission. This projects goals are to 

1)      Determine the origins of the aspergillosis outbreak in sea fans, using microsatellite markers,

2)      Evaluate the role of host resistance through development of immunological assays,

3)      Evaluate the role of environmental stressors in the outbreak, and

4)      Develop models for the within-individual and population level impacts of the disease.

 

My group has been involved primarily in items 3) and 4). We have developed a novel PDE model for the spread of a fungal pathogen within a coral host, which includes the hosts' natural immune response (mediated primarily by chemical signaling and mobile amoebocytes). The paper, currently in press at American Naturalist, shows that key factors determining the outcome of an infection are the rate at which fungus can consume host tissue and reproduce, and the rate at which the host can produce immune cells to replace those lost while battling the infection. Another important factor is whether the host is concurrently fighting several infections, each drawing on the limited supply of host immune cells. So coral vs. fungus is like long-term trench warfare: speed and ingenuity are much less important than the number of troops that can be thrown into battle. Consequently, any stresses that diminish even slightly the host's ability to regenerate immune cells, or its ability to chemically inhibit fungal growth and reproduction, could tip the balance in favor of the infection. There are many other lesion-forming infections of corals, so the results of this study may also be useful for understanding disease outbreaks in corals.

 

I am currently working with co-PI John Bruno (UNC-Chapel Hill) on development of an Integral Projection Model (IPM) for the population-level impacts of the disease. Population in which 60% of individuals are uninfected nonetheless have near-zero reproductive output, according to population surveys in the Caribbean by C.D. Harvell and K. Kim. The IPM shows that this is due to infection hitting the population with a double-whammy: reducing the number of individuals and their mean size. Only large, healthy individuals reproduce, so the individuals left alive and uninfected are mostly nonreproductive. More results soon…