I am an evolutionary microbiologist interested in the origins of aging at the cellular level. Since it is complicated to observe this process in multicellular organisms, my research uses bacteria as a model system. Bacterial populations are particularly suited for long-term observations and quantitative research: through single-cell microscopy and microfluidic techniques, I track bacterial lineages as they age and rejuvenate, following the progression of the aging phenotype over hundreds of generations.
   But how can bacteria show this replicative immortality and age at the same time? My past research addressed this conflict by demonstrating that bacterial aging leads to a state of equilibrium, rather than leading to mortality. Bacteria divide with asymmetry, giving more damage to one daughter. This produces a physiological distinction: one daughter ages, while the other rejuvenates. By tracking these lineages, we observed that asymmetry creates complex age-structure landscapes. When cells are exposed to environmental stress, aging bacteria are also more likely to die. Because rejuvenating bacteria are still replicating, this means that asymmetry creates patterns of mortality and immortality within populations.
   My current research focuses on the molecular sources of these patterns, investigating the contribution of deterministic asymmetry versus stochastic processes for bacterial phenotypes. I am also interested in addressing the implications of cellular aging for antibiotic survival and the emergence of other complex phenomena.