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Yersinia pestis , the agent of plague, forms a biofilm in its flea vector to enhance transmission.  Y .  pestis  biofilm development is positively regulated by  hmsT  and  hmsD , encoding diguanylate cyclases (DGCs) involved in synthesis of the bacterial second messenger c-di-GMP.  rcsA , encoding an auxiliary protein in Rcs phosphorelay, is nonfunctional in  Y .  pestis , while in  Yersinia pseudotuberculosis ,  rcsA  is functional and represses biofilms. Previously we showed that Rcs phosphorelay negatively regulates transcription of  hmsT  in  Y .  pestis  and its ancestor  Yersinia pseudotuberculosis . In this study, we show that Rcs positively regulates  hmsCDE  operon (encoding HmsD) in  Y .  pestis ; while in the presence of functional  rcsA , Rcs represses  hmsCDE  operon in  Y .  pseudotuberculosis . Loss of  rcsA 's function in  Y .  pestis  not only causes derepression of  hmsT  but also causes activation of  hmsD , which may account for the increased biofilm formation in  Y .  pestis . In addition, differential regulation of the two DGCs, HmsT and HmsD by Rcs may help  Y .  pestis  to adapt to different environment.

Differential regulation of the hmsCDE operon in Yersinia pestis and Yersinia pseudotuberculosis by the Rcs phosphorelay system