My research focuses on cooperation and antagonism in single species and two species interactions. The objective is to seek how ecological and evolutionary forces mold adaptations and drive their dynamics, and what this means for biological diversity. My laboratory uses a combination of mathematical modeling and experimental evolution with the system Pseduomonas fluorescens SBW25 - bacteriophage SBW252. We have several on-going projects, briefly described below.
Tradeoffs on different trophic levels. The main approach of this research is to see how two or more measurable traits co-vary across environments and how each impacts individual fitness. Given the enormous complexity of the molecular biology of individual growth and reproduction, adaptations to environmental conditions should create numerous opportunities for fitness covariation with resistance to natural enemies. Thus, resisting a specific pathogen for example need not entail specialized genes for this task, but rather mutations or recombinants of single or small numbers of genes associated with growth and reproduction, which confer greater net fitness in pathogen rich environments. This would be revealed by a tradeoff between resistance to pathogens and other life-history traits.
Cooperative polymorphism and tasking. We are interested in the role of cooperation and antagonism in population divergence and speciation. Intermediate steps in the divergence process may involve cooperative cycles or polymorphic states and we are currently addressing these possibilities through mathematical models and experimental evolution. The P. fluorescens system is ideal for this investigation since these bacteria form cooperative biofilms that show both cooperative cycles (biofilms are initially composed of cooperators and eventually are compromised by planktonic cheaters) and apparent polymorphic states (the investment in biofilm cohesion by wrinkly spreaders differs between different cell types). In a recent study led by Dr. Michael Brockhurst, we have found that biofilms diverging in the resource niches they exploit are more resistant to the invasion of cheats than more niche-homogeneous biofilms. This research suggests that resource specialization may be group selected, because these biofilms resist cheats and survive longer to create progeny biofims through budding or individual cell dispersal.
Mutational evolution. Mutation is one of the principal generators of phenotypic variation, and hence potential adaptation. Natural selection will mould mutation rates endogenously (the developmental biology of the organism itself), and exogenously (adaptation to the physical environment and to interactions with other organisms). Given the general importance of natural enemies in the population ecology and evolution of hosts or prey, one should expect specialized enemies to influence victim mutation rates and vice versa. Research in collaboration with Dr. Angus Buckling has demonstrated negative epistasis between resistance genes against phage and mutations in the P. fluorescens – 2 system. We are currently exploring these findings in greater detail for the more realistic situation of the persistent breakdown in DNA repair. We seek how this may influence the coevolution of life-history attributes and the temporal dynamics of epistasis. We are currently investigating how coevolutionary dynamics may impact mutation rates, our expectation being that under certain circumstances, increased rates can be selected via a hitchhiking mechanism.
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