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The transition between the planktonic state and the biofilm-associated state is a key developmental decision for pathogenic bacteria. Biofilm formation by  Yersinia pestis  is regulated by  hmsHFRS  genes (β-1, 6-N-acetyl-D-glucosamine synthesis operon) in its flea vector and  in vitro . However, the mechanism of biofilm formation in  Yersinia pseudotuberculosis  remains elusive. In this study, we demonstrate that the LysR-type regulator RovM inversely regulates biofilm formation and motility in  Y. pseudotuberculosis  by acting as a transcriptional regulator of these two functions. RovM is strongly induced during growth in minimal media but strongly repressed in complex media. On one hand, RovM enhances bacterial motility by activating the expression of FlhDC, the master regulator of flagellar genes, via the recognition of an operator upstream of the  flhDC  promoter. On the other hand, RovM represses β-GlcNAc production under nutrition-limited conditions, negatively regulating  hmsHFRS  expression by directly binding to the −35 element of its promoter. Compared to wild-type bacteria, the  rovM  mutant established denser biofilms and caused more extensive mortality in mice and silkworm larvae. These results indicate that RovM acts as a molecular switch to coordinate the expression of genes involved in biofilm formation and motility in response to the availability of nutrients.

A starvation-induced regulator, RovM, acts as a switch for planktonic/biofilm state transition in Yersinia pseudotuberculosis