The major goal of my research is to understand the evolution of conflict and cooperation. I'm especially interested in systems that involve bacteria and/or mobile genetic elements. Much of my work uses quantitative experimental approaches, including experimental evolution. I also use mathematical modelling to address conceptual issues, derive testable predictions, and interpret empirical results. I'm currently a postoc with Greg Velicer.
Microbial cooperation
An explosion of research in recent years has shown that many important microbial phenotypes--including traits involved in pathogenicity, metabolism, and development--are cooperative: they increase the fitness of other nearby cells or virions. What types of social interactions occur among microbes? What limits the spread of cheaters that benefit from a cooperative trait without paying the fitness cost of producing it?
Kin selection in microbes. A common explanation for the evolution of cooperation is that the benefits of cooperative traits preferentially go to individuals that carry the alleles for expressing it. With graduate students Peter Zee and Dave Van Dyken, I've derived a version of Hamilton's rule appropriate for microbes. This makes it possible to quantitatively test kin selection theory with real microbial data.
Horizontal gene transfer as a mechanism for enforcing cooperation. Many important bacterial genes, including those involved in antibiotic resistance and pathogen virulence, are carried by mobile genetic elements like plasmids and phage. Why should this be? I've shown that one potential explanation is that these genes code for cooperative traits and their mobility allows them to infect cheaters with the genes for cooperation.
Social selection in Myxococcus bacteria. We've found that Myxo development and sporulation involves multiple types of social interactions. Some strains cheat by contributing less to signalling molecules. Tan phase variants, however, outcompete yellow variants by becoming spores faster. Other strains actively suppress the development of their competitors. This suggests that Myxo fruiting bodies may be similar to social insect colonies, where reproductive success depends on a large number of traits, some of which are cooperative while others are primarily competitive. We're also working to determine the genetic basis of some of these traits.
Symbiosis and infectious disease
Symbioses are intimate associations between two species that can be good for both ("mutualism") or good for one species but not the other ("parasitism"). Unlike cooperation within species, where kin selection provides a unifying evolutionary principle, there is no well-supported theory that explains symbiosis. When do symbioses evolve to be mutualistic and when do they evolve to be parasitic? When do infectious diseases (one kind of symbiosis) evolve to be more harmful or less harmful?
Virulence evolution. One prominent hypothesis holds that horizontal transmission of pathogens between hosts selects for increased virulence while vertical transmission from a host to its offspring selects for decreased virulence. I tested this hypothesis using experimental evolution between E. coli bacteria and their antibiotic resistance plasmids. I found that the availability of uninfected cells failed to predict plasmid virulence. Instead, virulence was strongly correlated with the ability of evolved plasmids to reinfect already-infected cells. This suggests that within-host competition can play a dominant role in symbiont evolution.
Selfish genes. A long-standing challenge to the transmission mode hypothesis is the existence of selfish genetic elements such as meiotic drive genes and cytoplasmic sex ratio distorters. I've shown that these elements are in fact consistent with the hypothesis if one measures transmission from the perspective of host genes instead of host organisms. This theory also shows how to translate virulence theory across different levels of selection.
Last updated October 2009
