Some of the genes in question appear to code for cellular appendages, such as pili and flagella, suggesting that these proteinaceous fibrils are involved in the attachment or accumulation stages of biofilm development. When these genes are inactivated by mutation, the bacterium loses its ability to form a biofilm in vitro, and its virulence in some animal models of infection is reduced. Experiments such as these, in which a specific mutation in bacterial DNA results in the loss of biofilm-forming ability, provide a convincing link between the genetic code and the construction of a biofilm. Differential gene regulation has been demonstrated using reporter genes. And though much of the work remains unpublished, investigation of the role of intracellular signaling in biofilm formation has exploded.
Bacteria differentiate as they alight on a surface, expressing a distinct phenotype.
They synthesize communication molecules, reminiscent of the pheromones and hormones of insects and animals, to coordinate the building of microcolonies in a sophisticated 3-dimensional architecture. When bacterial clusters reach a critical size, the interaction of reaction and diffusion gives rise to gradients in the concentration of nutrients and metabolic products. This establishes a spectrum of environmental microniches with differing chemistries that permits the stable coexistence of different phenotypes of the same species and of wholly different microbial species. The collective strategy of life in a biofilm allows these bacterial communities to persist in the face of otherwise devastating antimicrobial challenges. Just as bacteria coordinate to initiate biofilm formation, they work in a concerted manner to dissolve microcolonies and release free-floating cells that can travel to colonize new environments.