I am an evolutionary biologist who uses fast-growing bacteria to study fundamental questions regarding the maintenance of organismal traits under relaxed selection. I am also interested in the evolutionary potential of these traits once selection is introduced. Specifically, I focus on the evolution of antibiotic resistance because of its profound relevance to public health.
Maintenance and evolutionary potential of antibiotic resistance traits during, and after relaxed selection
A population may encounter an environmental change that removes or reduces a selective pressure that was previously important for the maintenance of a trait. Adaptation to the new environment can therefore affect an organism’s fitness in its prior environment. These correlated responses may lead to the functional decay of unused traits over time. In most cases, the evolutionary processes driving these responses are hard to disentangle because one must rely on retrospective studies and historical inferences.
Bacteria have large population sizes, fast generation times, and they are amenable to freezing and revival. One can therefore observe evolution in action, directly compare ancestral and evolved forms, and simultaneously assess adaptation in one environment and correlated fitness responses in another. In our research, we use the long-term evolution experiment (LTEE) with Escherichia coli to examine correlated responses. Briefly, 12 replicate populations were founded from a single common ancestor. These populations have been independently evolving for 30 years and over 60,000 generations in a medium without antibiotics. We therefore address how a prolonged period of relaxed selection affects the maintenance of antibiotic resistance traits, and the potential of LTEE strains to evolve increased resistance.
Genetic basis for constraint on antibiotic resistance evolution in an LTEE population
The LTEE ancestor and evolved strains gain resistance in the presence of antibiotics. Though one evolved strain has significantly lower evolutionary potential compared to its common ancestor. Epistasis, whereby a mutation's effect depends upon the genetic background in which it appears, may explain this evolutionary constraint. To determine its genetic basis, my undergraduate mentee Jasper Gomez is using LTEE whole-genome sequence data to guide his examination of resistance evolution of ancestral and evolved isolates from throughout this population's history.