How bacteria regulate, assemble, and rotate flagella to swim in liquid media is reasonably well understood. Much less is known, however, about how some bacteria also use flagella to move over the tops of solid surfaces in a form of movement called swarming. As the focus of bacteriology changes from planktonic to surface environments, interest in swarming motility is on the rise. Here I review the requirements that define swarming motility in diverse bacterial model systems including an increase in the number of flagella per cell, secretion of a surfactant to reduce surface tension for spreading, and movement in multicellular groups rather than as individuals.

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SummaryWild strains of Bacillus subtilis are capable of forming architecturally complex communities of cells known as biofilms. Critical to biofilm formation is the eps operon, which is believed to be responsible for the biosynthesis of an exopolysaccharide that binds chains of cells together in bundles. We report that transcription of eps is under the negative regulation of SinR, a repressor that was found to bind to multiple sites in the regulatory region of the operon. Mutations in sinR bypassed the requirement in biofilm formation of two genes of unknown function, ylbF and ymcA , and sinI , which is known to encode an antagonist of SinR. We propose that these genes are members of a pathway that is responsible for counteracting SinRmediated repression. We further propose that SinR is a master regulator that governs the transition between a planktonic state in which the bacteria swim as single cells in liquid or swarm in small groups over surfaces, and a sessile state in which the bacteria adhere to each other to form bundled chains and assemble into multicellular communities.

SummarySwarming motility was identified and characterized in an undomesticated strain of Bacillus subtilis . Rapid surface migration was preceded by a cell densitydependent lag period, which could be eliminated if actively swarming cells were used as the inoculum. The leading edge of the swarm was characterized by multicellular rafts of highly flagellated cells. Flagellum biosynthesis and surfactant production were required for swarming. Swarming was not found in any of several standard laboratory strains. Laboratory strains are characteristically unable to produce surfactant, but such a strain remained unable to swarm even when surfactant was provided by extracellular complementation. We conclude that robust swarming is a feature of undomesticated B. subtilis and that this behaviour has been lost or attenuated in laboratory strains through the accumulation of multiple genetic defects.

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Many bacteria swim in liquid or swarm over solid surfaces by synthesizing rotary flagella. The same bacteria that are motile also commonly form non-motile multicellular aggregates held together by an extracellular matrix called biofilms. Biofilms are an important part of the lifestyle of pathogenic bacteria and it is assumed that there is a motility-to-biofilm transition wherein the inhibition of motility promotes biofilm formation. The transition is largely inferred from regulatory mutants that reveal the opposite regulation of the two phenotypes. Here we review the regulation of motility during biofilm formation in Bacillus, Pseudomonas, Vibrio, and Escherichia, and we conclude that the motility-to-biofilm transition, if necessary, likely involves two steps. In the short term, flagella are functionally regulated to either inhibit rotation or modulate the basal flagellar reversal frequency. Over the long term, flagellar gene transcription is inhibited and in the absence of de novo synthesis, flagella are likely diluted to extinction through growth. Both short term and long term control is likely important to the motility-to-biofilm transition to stabilize aggregates and optimize resource investment. We emphasize the newly discovered classes of flagellar functional regulators and speculate that others await discovery in the context of biofilm formation.

SummaryWild strains of the spore-forming bacterium Bacillus subtilis are capable of forming architecturally complex communities of cells. The formation of these biofilms is mediated in part by the 15-gene exopolysaccharide operon, epsA-O , which is under the direct negative control of the SinR repressor. We report the identification of an additional operon, yqxM-sipW-tasA , that is required for biofilm formation and is under the direct negative control of SinR. We now show that all three members of the operon are required for the formation of robust biofilms and that SinR is a potent repressor of the operon that acts by binding to multiple sites in the promoter region. Genome-wide analysis of SinR-controlled transcription indicates that the epsA-O and yqxM-sipW-tasA operons constitute many of the most strongly controlled genes in the SinR regulon. These findings reinforce the view that SinR is a master regulator for biofilm formation and further suggest that a principal biological function of SinR is to govern the assembly of complex multicellular communities.

Biofilms are multicellular aggregates of sessile bacteria encased by an extracellular matrix and are important medically as a source of drug-resistant microbes. In Bacillus subtilis, we found that an operon required for biofilm matrix biosynthesis also encoded an inhibitor of motility, EpsE. EpsE arrested flagellar rotation in a manner similar to that of a clutch, by disengaging motor force-generating elements in cells embedded in the biofilm matrix. The clutch is a simple, rapid, and potentially reversible form of motility control.