Cyclic di-GMP and the regulation of biofilm dispersion

Abstract

In nature, bacteria are primarily found as residents of surface-associated communities called biofilms. The formation of biofilms is a cyclical process that is initiated by single planktonic cells attaching to a surface, and comes full cycle when cells disperse from the mature biofilm to resume a planktonic lifestyle. Dispersion occurs in response to various signals and environmental cues, and results in surfaceattached organisms liberating themselves from matrix-encased biofilms, apparent by single cells actively escaping from the biofilm, leaving behind eroded biofilms and microcolonies having central voids. Given the cyclic process of biofilm formation, it is not surprising that dispersion, like biofilm formation, is coincident with significant changes in the levels of the second messenger cyclic di-GMP. However, dispersion is not simply a reversion from the biofilm lifestyle to the planktonic mode of growth, as dispersed cells have been described as having a phenotype that is distinct from planktonic and biofilm cells. Using primarily the pathogen P. aeruginosa as example, this chapter provides an up-to-date compendium of cyclic di-GMP pathways connected to biofilm dispersion, including how sensing a diverse array of dispersion cues leads to the destruction of cyclic di-GMP, the escape from the biofilm matrix, and the appropriate phenotypic responses associated with dispersed cells.