We use a combination of computer modeling and laboratory experimentation to study ecological and evolutionary processes. Ecological and evolutionary studies are often difficult to investigate because they occur slowly over long periods of time. Computer models can speed up time, but we also take advantage of the fact that microbes, bacteria and viruses provide that same advantage because of their short generation times. Furthermore, they can be easily cultured in the laboratory under controlled conditions. However, we also realize that too much control can be dangerous because an experiment that is too controlled becomes artificial and not much more than a simulation. And a simulation is always more easily obtained from a computer model. Thus, we are careful to design experiments that teach us more than a computer model. We make sure that the experiments allow us to measure an unknown that could not be determined a priori from a computer model. We have used microbial systems to study topics ranging from the ecology of host-parasite co-existence and the evolution of sex, mutation rates, transposable elements, group and individual adaptations, game theory strategies, Fisher’s Geometric Model of Adaptive Evolution, deleterious and compensatory mutations. As new information or interests develop, we often revisit older topics or explore new ones.
Time lapse photograph E. coli cells descending from a single cell. By recording division of all cells via time lapse, the doubling time or life history fitness of every individual in a population can be determined.
Our current research focuses on evolution of microbial aging or senescence, which grew out of our interest in genetic damage or mutations. Because most mutations are deleterious, they lead to fitness loss unless removed by natural selection. The transmission of mutations from mother to daughter is governed by well the well known rules of genetic inheritance and assortment. However, non-genetic or phenotypic damage can also decrease fitness and, unlike mutations, the transmission rules for phenotypic damage are not well understood. If a mother cell has ten units of phenotypic damage, for example ten proteins damaged by oxidation, should she distribute the damage evenly between her two daughters or give all ten units to one daughter and none to the other? Our theoretical models have shown that a lineage maximizes its fitness by allocating all the damage to a single daughter. Thus, asymmetry should evolve and the daughter receiving all or more damage should senesce over time. Time lapse photography of dividing cells has already shown that bacteria divide asymmetrically. We are now making our own time lapse series to test more directly the prediction of our models.
Lin Chao received his Ph.D. from the University of Massachusetts, Amherst. He was an NIH postdoctoral fellow at Princeton University. He is the recipient of the Associate Student Government Faculty Teaching Award.