Quorum sensing is a cell-cell communication mechanism employed by bacteria to regulate population-density dependent behaviour. It is usually assumed that quorum sensing triggers a coordinated response from a population of cells that benefits the bacteria as a community. For example, a population of pathogenic bacteria that times the onset of virulence factor production to occur when population number has grown sufficiently is more likely to cause a successful infection than one that attacks the host immediately upon entry. However, the increasing number of quorum-sensing systems now discovered across the bacterial kingdom has begun to reveal more complex roles for quorum sensing in regulating population behaviour.

Comparing the agr-type quorum-sensing system of the pathogenic bacterium Staphylococcus aureus (responsible for an enormous array of medical problems, from minor skin infections to toxic shock syndrome, for example) and Clostridium acetobutylicum (a non-pathogenic bacterium notable for its production of biofuel-related solvents), we investigate how only slight modifications to the quorum-sensing network architecture may be responsible for determining whether a population behaves uniformly or is divided into phenotypically distinct subpopulations. We illustrate how this corresponds neatly to the putative roles for quorum sensing in each of these organisms: virulence factor production for S. aureus and sporulation for C. acetobutylicum.