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Maintaining motile reserves
During biofilm formation, bacterial cells switch from a motile planktonic state to a matrix-producing, adherent state. Although bacterial biofilms are generally sessile, some, such as those formed by Bacillus subtilis, can spread to overtake and kill neighboring colonies of competitor species. Steinberg et al. found that a motile subpopulation of cells within B. subtilis biofilms was required for the biofilms to spread over foreign objects. This process required the matrix protein TasA, which stimulated a subset of cells within the biofilm to revert from a matrix-producing state to a motile state, thus ensuring that the colony could spread.
Abstract
In nature, bacteria form biofilms—differentiated multicellular communities attached to surfaces. Within these generally sessile biofilms, a subset of cells continues to express motility genes. We found that this subpopulation enabled Bacillus subtilis biofilms to expand on high-friction surfaces. The extracellular matrix (ECM) protein TasA was required for the expression of flagellar genes. In addition to its structural role as an adhesive fiber for cell attachment, TasA acted as a developmental signal stimulating a subset of biofilm cells to revert to a motile phenotype. Transcriptomic analysis revealed that TasA stimulated the expression of a specific subset of genes whose products promote motility and repress ECM production. Spontaneous suppressor mutations that restored motility in the absence of TasA revealed that activation of the biofilm-motility switch by the two-component system CssR/CssS antagonized the TasA-mediated reversion to motility in biofilm cells. Our results suggest that although mostly sessile, biofilms retain a degree of motility by actively maintaining a motile subpopulation.
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