A bacterial population that initially consists of a single clone can evolve into a population teeming with many, whether or not the surrounding environment is structured, and whether or not resource levels are constant or fluctuating. Emergence of genetic complexity, measured as functional information, has been variously attributed to balancing selection, clonal interference and/or clonal reinforcement arising from either antagonistic or synergistic interactions among evolving lineages. Using a combination of theory and experiment, we seek to define the boundary conditions under which one causal mechanism prevails over another. These investigations illuminate the process of adaptive evolution in other populations that originate as a single clone: those that give rise to cancer and those that bring about chronic infectious disease.