An intricate network of regulators controls biofilm formation and colonization by Vibrio fischeri

Abstract

The initial encounter between a microbe and its host can dictate the success of the interaction, be it symbiosis or pathogenesis. This is the case, for example, in the symbiosis between the bacterium Vibrio fischeri and the squid Euprymna scolopes, which proceeds via a biofilm-like bacterial aggregation, followed by entry and growth. A key regulator, the sensor kinase RscS, is critical for symbiotic biofilm formation and colonization. When introduced into a fish symbiont strain that naturally lacks the rscS gene and cannot colonize squid, RscS permits colonization, thereby extending the host range of these bacteria. RscS controls biofilm formation by inducing transcription of the symbiosis polysaccharide (syp) gene locus. Transcription of syp also requires the sigma(54)-dependent activator SypG, which functions downstream of RscS. In addition to these regulators, SypE, a response regulator that lacks an apparent DNA binding domain, exerts both positive and negative control over biofilm formation. The putative sensor kinase SypF and the putative response regulator VpsR, both of which contribute to control of cellulose production, also influence biofilm formation. The wealth of regulators and the correlation between biofilm formation and colonization adds to the already considerable utility of the V. fischeri-E. scolopes model system.

Figure 1. Model for control of biofilm formation in V. fischeri

Depicted here is a model based on current data regarding the potential roles of the syp regulators. The sensor kinase RscS acts upstream of SypG, presumably serving as a phosphodonor in response to some as-yet unidentified environmental signal, perhaps from the squid. Once phosphorylated, SypG is predicted to directly bind to sequences upstream of each of 4 syp operons to activate syp transcription by σ⁵⁴-containing RNA polymerase. The Syp proteins contribute to biofilm formation in culture, including the formation of wrinkled colonies and pellicles, as well as in situ biofilm formation and colonization. RscS overproduction also appears to inactivate SypE, which inhibits biofilm formation induced by overproduction of SypG at a level downstream from syp transcription; how RscS inactivates SypE is as yet unknown. Biofilm formation can be also induced by overexpression of a sypF allele with increased activity (SypF1) in a manner that depends in part on SypG and SypE, and in part on VpsR, which promotes cellulose biosynthesis.